Request
Zoe
he has not answered. Can anyone else please provide an answer to the
following evolutionary scenario?
Can you trace the pathway of how chimps and humans manage to
produce offspring as they first separate from their common ancestor?
The common ancestor has, let's say, 23 pairs of chromosomes. A rare
"beneficial mutation" causes an offspring to be born with an extra
pair of chromosomes. He is the forerunner of the chimp. Where does
the human ancestor come in? Does the common ancestor also produce an
offspring with 23 pairs of chromosomes, but with some other rare
"beneficial mutation" that takes the offspring, now ancestor to
humans, in a different direction?
Here's your budding tree.
common ancestor Chimp ancestor (single individual)
_____________________/
\
Human ancestor (single individual)
Can you take it from there? What's the pathway? At this point, can
the chimp ancestor still interbreed with either the common ancestor or
with the human ancestor? It has to interbreed with something in order
to produce more offspring after its own kind, so where does the
partner come from?
If there is no reasonable and/or specific answer as to a possible
pathway for the above to happen, then why on earth do evolutionists
make such strong claims that it happened? And why do they lambast
anyone who dares to question their scenario?
Steven J.
"Zoe" <muz...@aol.com> wrote in message
news:ho5ud1tiqh4h94opl...@4ax.com...
> Following is a portion of a post in response to Howard Hershey, which
> he has not answered. Can anyone else please provide an answer to the
> following evolutionary scenario?
>
> Can you trace the pathway of how chimps and humans manage to
> produce offspring as they first separate from their common ancestor?
>
> The common ancestor has, let's say, 23 pairs of chromosomes. A rare
> "beneficial mutation" causes an offspring to be born with an extra
> pair of chromosomes. He is the forerunner of the chimp. Where does
> the human ancestor come in? Does the common ancestor also produce an
> offspring with 23 pairs of chromosomes, but with some other rare
> "beneficial mutation" that takes the offspring, now ancestor to
> humans, in a different direction?
>
of humans and chimps had 24 pairs of chromosomes. First, chimps, gorillas,
and orangutans all have 24 pairs of chromosomes (which makes it seem more
likely that was the number of the last common ancestor of great apes, and
continued until it was reduced in the human lineage). Second, while all
chromosomes have a centromere in the center and telomeres at the end, human
chromosome two has a vestigial centromere and telomere embedded in the
chromosome itself, suggesting that it was formed by a fusion of two
chromosomes. Indeed, there are two separate chromosomes in chimps that are
very similar in sequence to two "halves" of human chromosome 2.
By the way, although you didn't explicitly ask, the okapi (a rare,
short-necked giraffe) species has individuals with 22 pairs of chromosomes,
23 pairs, and even 22.5 pairs (for 45 chromosomes in all -- in which case
two chromosomes from one parent must be paired with one -- fused --
chromosome from the other parent). So a mutation that produced the first
human with a chromosome 2 (rather than the ancestral chromosomes 2a and 2b)
would not have prevented that individual from mating successfully. Or, take
the case of Przewalski's horse and the domestic horse: domestic horses, like
their human breeders, have one fewer chromosome pairs than their wild
ancestors, due, apparently, to a chromosomal fusion -- but domestic and
Przewalski's horses can still interbreed to produce fertile offspring. In
other cases (e.g. "chromosomal races" of mice), having different chromosome
numbers reduces interfertility.
There is no reason to suppose that the difference in chromosome numbers
started with the last common ancestor; it may well have been much more
recent, long after the human line had separated from the chimp line.
There's no particular reason, for that matter, to suppose that the human
line started out with some particular beneficial mutation, rather than our
ancestors simply moving into a different part of Africa from Cheetah's
ancestors, so that they could no longer interbreed (geographical separation
prevented any new beneficial -- or neutral or harmful -- mutations in the
hominin line from entering the chimp gene pool).
>
> Here's your budding tree.
>
>
> common ancestor Chimp ancestor (single individual)
> _____________________/
> \
> Human ancestor (single individual)
>
No, surely the branching involved entire breeding populations -- one band,
or a few bands, of apes moving into a new territory far from the lands where
other members of their species lived. As noted, at the branch point, both
populations would have been apes of the same species; they wouldn't become
different species until *after* the branch point, after geographical
separation left them free to evolve in two different directions. Remember
that, just as there was no "first French speaker" struggling to make himself
understood in a nation of classical Latin speakers, so there was no "first
human" or "first chimpanzee," but only a gradual change over many
generations from the same ancestral species.
>
> Can you take it from there? What's the pathway? At this point, can
> the chimp ancestor still interbreed with either the common ancestor or
> with the human ancestor? It has to interbreed with something in order
> to produce more offspring after its own kind, so where does the
> partner come from?
>
Most evolutionists hold that most speciation events are "allopatric,"
meaning that they occur *after* the ancestral population has split into two
groups that could interbreed if they met, but which no longer meet up.
Afterwards, mutation, genetic drift, and selection to different environments
gradually change the populations into different species. No particular
mutation (unless you count polyploidy) is likely to produce a new species.
A better (though still oversimplified) approach would be to think of a
whole series of mutations, some beneficial, most neutral (but they still
made us different from chimps), that each made the bearer a tiny bit more
"human" (or, in the other lineage, a tiny bit more "chimp"). No single
gene would have made its bearer much different from other members of his
species, or unable to interbreed with them.
It doesn't seem likely that a modern human could (or at least would)
interbreed with a modern chimp, but presumably five million years ago, our
ancestors were just a tiny bit more "human" than the ancestors of modern
chimps. They probably could have produced fertile offspring with the chimp
ancestors, but as noted, they lived in different parts of Africa and no
longer met.
By the way, polyploidy is duplication of the entire genome; plants speciate
this way all the time, but it's rarer for animals (though there are strongly
supported examples for frogs, rodents, and other vertebrates; presumably,
they can't form a new species unless they can either reproduce
parthenogenically, or unless polyploidy happens often enough that eventually
it produces two members of the same species at the same time and place).
But this has nothing to do with how humans split off from apes.
>
> If there is no reasonable and/or specific answer as to a possible
> pathway for the above to happen, then why on earth do evolutionists
> make such strong claims that it happened? And why do they lambast
> anyone who dares to question their scenario?
>
-- Steven J.
Mike Dworetsky
diverge from a common ancestor that I would like to see it mounted as a Post
of the Month. "No first Frenchman" indeed.
--
Mike Dworetsky
(Remove "pants" spamblock to send e-mail)
"Steven J." <sjt195...@nts.link.net.INVALID> wrote in message
news:11du954...@corp.supernews.com...
zawa...@yahoo.com
Ce qui? Aucun premier Français?
Cheezits
> This is such a clear and readable explanation of the way in which
> species diverge from a common ancestor that I would like to see it
> mounted as a Post of the Month. "No first Frenchman" indeed.
I agree. I had wondered about that chromosome question myself.
Sue
--
"It's not smart or correct, but it's one of the things that
make us what we are." - Red Green
John Harshman
> Following is a portion of a post in response to Howard Hershey, which
> he has not answered. Can anyone else please provide an answer to the
> following evolutionary scenario?
>
> Can you trace the pathway of how chimps and humans manage to
> produce offspring as they first separate from their common ancestor?
>
> The common ancestor has, let's say, 23 pairs of chromosomes. A rare
> "beneficial mutation" causes an offspring to be born with an extra
> pair of chromosomes. He is the forerunner of the chimp. Where does
> the human ancestor come in? Does the common ancestor also produce an
> offspring with 23 pairs of chromosomes, but with some other rare
> "beneficial mutation" that takes the offspring, now ancestor to
> humans, in a different direction?
There are several problems with this scenario already. First, you assume
that the common ancestor is a single individual when it's really a
population or species. Second, you assume this chromosomal mutation is
beneficial, for which there is no evidence. Third, you assume that the
mutation in question was a fission in the chimp line, when it was
instead a fusion in the human line. Fourth, you assume that the mutation
happened in the common ancestor, when it almost certainly happened some
time after the human and chimp lineages separated. Fifth, you assume
that this mutation had something to do with making us human, when it's
most likely to be irrelevant.
> Here's your budding tree.
>
>
> common ancestor Chimp ancestor (single individual)
> _____________________/
> \
> Human ancestor (single individual)
I'm afraid your ASCII graphics have misfired. But there is no single
individual involved here, just populations that become isolated
(geographically at first) and diverge from each other.
> Can you take it from there? What's the pathway? At this point, can
> the chimp ancestor still interbreed with either the common ancestor or
> with the human ancestor? It has to interbreed with something in order
> to produce more offspring after its own kind, so where does the
> partner come from?
The partner comes from other members of its population. At some time in
the past, the common ancestral species became split into two
populations, geographically isolated from each other. At this point they
began diverging. They may in fact have begun with slightly different
gene pools, because of locaal differences that already existed, as is
common in many species with large ranges. The environments in the two
now-isolated parts of the original species range may have been somewhat
different too, in which case selection would speed divergence. But in
any case, drift would cause divergence too. After a while, sooner if
selection is operating and later if only drift is operating, the
descendants, if put together, would no longer recognize each other as
potential mates. And that's speciation.
As for the chromosomal mutation, that's just one of the changes that
happened in the human lineage. It began as a single mutation in a single
individual, and for one reason or another increased in frequency in that
population until it reached fixation, and now all humans have only 46
chromosomes instead of 48.
Chromosomal fusion, by the way, does not prevent interbreeding with
other members of the population that have unfused chromosomes. If you
look on the web, you will find several examples of species with
chromosomal polymorphisms of this sort.
> If there is no reasonable and/or specific answer as to a possible
> pathway for the above to happen, then why on earth do evolutionists
> make such strong claims that it happened? And why do they lambast
> anyone who dares to question their scenario?
If their basis for questioning it is a complete misunderstanding of the
facts, then lambasting is entirely appropriate.
Zoe
<sjt195...@nts.link.net.INVALID> wrote:
>
>"Zoe" <muz...@aol.com> wrote in message
>news:ho5ud1tiqh4h94opl...@4ax.com...
>> Following is a portion of a post in response to Howard Hershey, which
>> he has not answered. Can anyone else please provide an answer to the
>> following evolutionary scenario?
>>
>> Can you trace the pathway of how chimps and humans manage to
>> produce offspring as they first separate from their common ancestor?
>>
>> The common ancestor has, let's say, 23 pairs of chromosomes. A rare
>> "beneficial mutation" causes an offspring to be born with an extra
>> pair of chromosomes. He is the forerunner of the chimp. Where does
>> the human ancestor come in? Does the common ancestor also produce an
>> offspring with 23 pairs of chromosomes, but with some other rare
>> "beneficial mutation" that takes the offspring, now ancestor to
>> humans, in a different direction?
>>
>For a couple of reasons, it seems more likely that the last common ancestor
>of humans and chimps had 24 pairs of chromosomes. First, chimps, gorillas,
>and orangutans all have 24 pairs of chromosomes (which makes it seem more
>likely that was the number of the last common ancestor of great apes, and
>continued until it was reduced in the human lineage).
is this a principle, that majority determines which comes first? In
comparing genomes in species that are supposed to be related, if there
are more life forms with the same number of chromosomes, then is that
taken to mean, as a rule, they had to be ancestors to those with a
lesser number of chromosomes?
If not, then we can discard your first reason.
> Second, while all
>chromosomes have a centromere in the center and telomeres at the end, human
>chromosome two has a vestigial centromere and telomere embedded in the
>chromosome itself, suggesting that it was formed by a fusion of two
>chromosomes. Indeed, there are two separate chromosomes in chimps that are
>very similar in sequence to two "halves" of human chromosome 2.
this would appear, on its surface, to be a more convincing reason to
conclude that humans and chimps have a common ancestor (though you
have not yet addressed how fusion affects fertility or the parallel
meaning, if any, attached to chromosome fusion in mice.)
That said, the latest evidence in genome comparison between chimps and
humans reveal an 83% difference between chimp chromosome 22 and human
chromosome 21 (chimp chromosome 22 is said to be the ortholog of human
chromosome 21.) And even though there appears to be 99% similarity
between the DNA of humans and chimps, the recombination hot spots have
turned out to be almost completely different. Apparently, then, DNA
sequences, even though highly similar, do not determine biological
function.
It's like comparing the recipes for two cakes. They both use 99%
similar ingredients -- flour, sugar, butter, eggs. Does this
similarity mean that both cakes came from the same batter? Not
necessarily. Not even probably. The more reasonable assumption is
that both cakes were created in their own right, from different
recipes, but using similar ingredients.
>By the way, although you didn't explicitly ask, the okapi (a rare,
>short-necked giraffe) species has individuals with 22 pairs of chromosomes,
>23 pairs, and even 22.5 pairs (for 45 chromosomes in all -- in which case
>two chromosomes from one parent must be paired with one -- fused --
>chromosome from the other parent).
would you have references, by any chance, to studies that have
followed the interbreeding of these subspecies of opaki? Have they
tried to interbreed an opaki with 22 pairs of chromosomes with an
opaki that has 23 pairs of chromosomes? Or do opakis with 22 pairs of
chromosomes breed only with those that have 22 pairs of chromosomes,
and so on?
> So a mutation that produced the first
>human with a chromosome 2 (rather than the ancestral chromosomes 2a and 2b)
>would not have prevented that individual from mating successfully.
I'm not sure that that is a hard-and-fast conclusion, considering that
there is no evidence today that humans with chromosome 2 can
interbreed with chimps with chromosomes 2a and 2b. If they can't
today, why speculate that they could have at one time, unless you have
evidence that such a thing is possible?
> Or, take
>the case of Przewalski's horse and the domestic horse: domestic horses, like
>their human breeders, have one fewer chromosome pairs than their wild
>ancestors, due, apparently, to a chromosomal fusion -- but domestic and
>Przewalski's horses can still interbreed to produce fertile offspring. In
>other cases (e.g. "chromosomal races" of mice), having different chromosome
>numbers reduces interfertility.
if you are comparing the horse scenario to the human/chimp scenario,
you would need to explain why the domestic horse can still breed
successfully with their wild ancestor, the Przewalski horse, and yet
humans cannot breed with their supposed wild ancestor, the ape.
>There is no reason to suppose that the difference in chromosome numbers
>started with the last common ancestor; it may well have been much more
>recent, long after the human line had separated from the chimp line.
>There's no particular reason, for that matter, to suppose that the human
>line started out with some particular beneficial mutation, rather than our
>ancestors simply moving into a different part of Africa from Cheetah's
>ancestors, so that they could no longer interbreed (geographical separation
>prevented any new beneficial -- or neutral or harmful -- mutations in the
>hominin line from entering the chimp gene pool).
>>
>> Here's your budding tree.
>>
>>
>> common ancestor Chimp ancestor (single individual)
>> _____________________/
>> \
>> Human ancestor (single individual)
>>
>No, surely the branching involved entire breeding populations -- one band,
>or a few bands, of apes moving into a new territory far from the lands where
>other members of their species lived. As noted, at the branch point, both
>populations would have been apes of the same species; they wouldn't become
>different species until *after* the branch point, after geographical
>separation left them free to evolve in two different directions. Remember
>that, just as there was no "first French speaker" struggling to make himself
>understood in a nation of classical Latin speakers, so there was no "first
>human" or "first chimpanzee," but only a gradual change over many
>generations from the same ancestral species.
okay, so I'll redraw the ancestral lines as follows, according to your
explanation.
Chimp ancestor population (24chrm)
common ancestor (24 chrm) /_____________________
___________________________/
\
\
Human ancestor population (24chrm)
At this point, there is as yet no change in the genetic makeup of
either the chimp ancestor population or the human ancestor population.
The only change is in geographical location which prevents Population
A (containing a potential chimp ancestor) from interbreeding with
Population B (containing a potential human ancestor).
Right so far?
Okay, so focusing now on the human ancestor population:
Human ancestor population (24chrm)
______________________________ /??
What happens at this point? A fusion occurs in a single individual in
this population, supposedly, right? I take it that the proposed rare
beneficial mutations do not hit several members of the population at
the same time? Otherwise they wouldn't be rare.
Okay, so we now have a population of 24chrm members and one member's
chromosomes 2a and 2b fuse into a single chromosome, forming
chromosome 2 of the human ancestor's set of chromosomes.
Supposedly, this 23chrm member of the 24chrm population can continue
to interbreed with the 24chrm members, producing offspring that may or
may not carry this 23chrm set. How does selection work in this case?
Has it been demonstrated that Chromosome 2 in humans makes them
distinctly different from apes, and gives them a distinct selective
advantage? If not, it would be predicted that 23chrm members of the
population would not necessarily increase but instead, as, they
continue to interbreed, the 24chrm members will dominate because they
are more in abundance, and the supposedly advantageous and distinct
Chromosome 2 will die out and be lost to the population.
That would be one scenario. There's another. Looking at comparisons
of human chromosome 2 and chimp chromosomes 2a and b, except for where
the fusion supposedly occurs, the chromosomes appear to be physically
identical. Problem here is which direction to go in giving value to
the similarities.
If the similarities mean that both human chromosome 2 and chimps
chromosomes 2a and b will produce biological similarities, then what
is there to choose from, selection wise, in order to give the
advantage to Chromosome 2 in humans?
But if, as research reveals (as recently as February, 2005),
recombination hot spots on human chromosome 21, supposedly orthologous
to chimp chromosome 22, are 83% different, and 17% similar -- then
even though human Chromosome 2 and Chimp Chromosomes 2a and b appear
to be almost identical, this apparent similarity may not be real after
all.
See:
http://www.admin.ox.ac.uk/po/050214.shtml
>> Can you take it from there? What's the pathway? At this point, can
>> the chimp ancestor still interbreed with either the common ancestor or
>> with the human ancestor? It has to interbreed with something in order
>> to produce more offspring after its own kind, so where does the
>> partner come from?
>>
>Most evolutionists hold that most speciation events are "allopatric,"
>meaning that they occur *after* the ancestral population has split into two
>groups that could interbreed if they met, but which no longer meet up.
>Afterwards, mutation, genetic drift, and selection to different environments
>gradually change the populations into different species. No particular
>mutation (unless you count polyploidy) is likely to produce a new species.
>A better (though still oversimplified) approach would be to think of a
>whole series of mutations, some beneficial, most neutral (but they still
>made us different from chimps),
no, no, no, you can't claim neutral mutations as changes that make us
different from chimps. If humans become different, it would be
because change (or mutation, as you call it) has occurred. No change,
no difference. Neutral "mutations" cannot be counted to make a
difference between humans and chimps. So once again you are left with
trying to have the rare "beneficial" mutation carry the entire weight
of your evolutionary theory.
> that each made the bearer a tiny bit more
>"human" (or, in the other lineage, a tiny bit more "chimp"). No single
>gene would have made its bearer much different from other members of his
>species, or unable to interbreed with them.
in which case, selection has nothing to work on, does it?
>It doesn't seem likely that a modern human could (or at least would)
>interbreed with a modern chimp, but presumably five million years ago, our
>ancestors were just a tiny bit more "human" than the ancestors of modern
>chimps.
how can a life form be a tiny bit more human before it becomes human?
> They probably could have produced fertile offspring with the chimp
>ancestors, but as noted, they lived in different parts of Africa and no
>longer met.
I note the use of "probably" here.
snip>
Steven J.
came first. "Parsimony," in this case, means accounting for the observed
pattern with the fewest postulated entities -- in this case, mutations. If
the last common ancestor (LCA) of African apes had 23 chromosome pairs, then
we need two mutations -- one to give the gorillas 24 pairs, and one to give
the chimps 24 pairs -- to account for the observed distribution. If we
assume that the African ape LCA had 24 pairs, but the human-chimp LCA had 23
pairs, then we still need two mutations: one to reduce the number of pairs
after the human-chimp line splits from gorillas, and one to increase the
number of pairs in chimps after the human and chimp lines split. If we
assume that both the African ape and human-chimp LCA had 24 pairs, then we
need only one mutation to explain the difference (after the human-chimp
split). Of course, in some cases, parsimony will be *wrong* (nature isn't,
as far as anyone knows, trying to keep mutations to a minimum), but it seems
a good approximation most of the time.
>
> If not, then we can discard your first reason.
>
>> Second, while all
>>chromosomes have a centromere in the center and telomeres at the end,
>>human
>>chromosome two has a vestigial centromere and telomere embedded in the
>>chromosome itself, suggesting that it was formed by a fusion of two
>>chromosomes. Indeed, there are two separate chromosomes in chimps that
>>are
>>very similar in sequence to two "halves" of human chromosome 2.
>
> this would appear, on its surface, to be a more convincing reason to
> conclude that humans and chimps have a common ancestor (though you
> have not yet addressed how fusion affects fertility or the parallel
> meaning, if any, attached to chromosome fusion in mice.)
>
>
> That said, the latest evidence in genome comparison between chimps and
> humans reveal an 83% difference between chimp chromosome 22 and human
> chromosome 21 (chimp chromosome 22 is said to be the ortholog of human
> chromosome 21.) And even though there appears to be 99% similarity
> between the DNA of humans and chimps, the recombination hot spots have
> turned out to be almost completely different. Apparently, then, DNA
> sequences, even though highly similar, do not determine biological
> function.
>
83% of the genes have at least one nucleotide different between the two
species, that is perfectly consistent with a 99% sequence similarity between
the two chromosomes. Suppose (these figures are illustrative only; do not
assume they reflect actual measurements of the chromosome) that two
chromosomes in different species have 100 genes each. Suppose each gene has
300 nucleotides, and that for each gene two nucleotides differ between the
two species. That would mean that on this chromosome, 100% of the genes are
(slightly) different from their homologues in the other species, but that
overall sequence similarity is over 99%. But certainly minor differences in
DNA sequence can produce major changes in function, and certainly genes by
themselves do not determine everything that happens in an organism.
>
> It's like comparing the recipes for two cakes. They both use 99%
> similar ingredients -- flour, sugar, butter, eggs. Does this
> similarity mean that both cakes came from the same batter? Not
> necessarily. Not even probably. The more reasonable assumption is
> that both cakes were created in their own right, from different
> recipes, but using similar ingredients.
>
minor ingredients) may strongly indicate origin from the same batter. At
least, this line of reasoning is commonly used in forensic science for
bullet fragments and dirt samples. But in any case, a closer analogy to DNA
would be the exact wording of the recipes themselves -- especially if both
recipes shared the same mispellings of the same words in the same order, and
had bits of text that were alike but didn't seem to have anything to do with
the actual recipe (like, e.g. the pseudogenes and endogenous retroviruses
chimps and humans share).
By the way, why is it more reasonable, even if we don't know for sure, to
suppose that the cakes were created from different recipes and different
batter? Certainly a baker is capable of making one big batch of batter and
making lots of cakes from it. And a Creator, I would suppose, is perfectly
capable of making many species from a single ancestral population, as He
made (according to the Bible) many nations from one original human
population.
>
>>By the way, although you didn't explicitly ask, the okapi (a rare,
>>short-necked giraffe) species has individuals with 22 pairs of
>>chromosomes,
>>23 pairs, and even 22.5 pairs (for 45 chromosomes in all -- in which case
>>two chromosomes from one parent must be paired with one -- fused --
>>chromosome from the other parent).
>
> would you have references, by any chance, to studies that have
> followed the interbreeding of these subspecies of opaki? Have they
> tried to interbreed an opaki with 22 pairs of chromosomes with an
> opaki that has 23 pairs of chromosomes? Or do opakis with 22 pairs of
> chromosomes breed only with those that have 22 pairs of chromosomes,
> and so on?
>
Okapis have no known subspecies; the variant chromosome numbers do not
correspond to racial or habitat differences. And, apparently, they
interbreed freely with okapis with different numbers of chromosomes and
produce fertile offspring. Google turns up a few scholarly articles on
"chromosomal polymorphism" in okapis and other species, and this appears, in
okapis and some other species, to work like any other polymorphism (that is,
it no more affects interbreeding than the difference between, say, type A
and type O blood, or blue and brown eyes).
>
>> So a mutation that produced the first
>>human with a chromosome 2 (rather than the ancestral chromosomes 2a and
>>2b)
>>would not have prevented that individual from mating successfully.
>
> I'm not sure that that is a hard-and-fast conclusion, considering that
> there is no evidence today that humans with chromosome 2 can
> interbreed with chimps with chromosomes 2a and 2b. If they can't
> today, why speculate that they could have at one time, unless you have
> evidence that such a thing is possible?
>
There's no evidence that chimps with chromosomes 2a and 2b can interbreed
with gorillas with chromosomes 2a and 2b. They've spent seven million years
or more evolving in different directions (not just in obvious anatomical
ways, but in more subtle ones). For all either of us knows, hominins (the
human side of the human-chimp lineage) and panins (the chimp side) stopped
being interfertile before the chromosome fusion happened in the hominin
line. I doubt that chromosome number per se is much of a guide to
interfertility.
But again, horse subspecies with different numbers of chromosomes are
interfertile. Okapis with a rather recent mutation that produced a fused
chromosome are interfertile. I'm speculating that what is known to happen
in several species today could have happened in other species at other
times; it seems a safe enough speculation.
>
>> Or, take
>>the case of Przewalski's horse and the domestic horse: domestic horses,
>>like
>>their human breeders, have one fewer chromosome pairs than their wild
>>ancestors, due, apparently, to a chromosomal fusion -- but domestic and
>>Przewalski's horses can still interbreed to produce fertile offspring. In
>>other cases (e.g. "chromosomal races" of mice), having different
>>chromosome
>>numbers reduces interfertility.
>
> if you are comparing the horse scenario to the human/chimp scenario,
> you would need to explain why the domestic horse can still breed
> successfully with their wild ancestor, the Przewalski horse, and yet
> humans cannot breed with their supposed wild ancestor, the ape.
>
Well, I'm not sure it's been conclusively demonstrated that we *can't*
interbreed with chimps, but assuming that we can't, our ancestors split from
theirs about six million years ago; that's a lot of time to evolve barriers
to interbreeding (starting with we probably look a lot uglier and less sexy
to each other than the two horse subspecies do). The ancestors of
Przewalski's horse separated from those of modern horses much more recently
(60,000 years ago? 6000 years ago? more recently still -- perhaps not
until humans started domesticating horses?). Reproductively isolated
populations evolve intersterility by degrees, over time, and at varying
rates.
Please try to understand: there is no reason to suppose that the difference
in chromosome number caused he split between the hominin and panin lines, or
happened at the same time. Now, it's possible that it occurred in the
human-chimp LCA, and the 23-pair version simply died out among chimps and
survived and became "fixed" (present in 100% of the population) in humans.
If this is the case, then there was a time when it wasn't a peculiarly
"human" trait, any more than type A blood (which is also a polymorphism
present in both humans and chimps) is, and individuals with both chromosome
numbers could interbreed freely. Or perhaps, as I suggested in my earlier
post, the chromosomal polymorphism arose after the human-chimp split, and no
chimp ancestor ever had that particular chromosomal fusion. I don't know of
any strong reason to prefer either possibility.
Right, except that population A contains many potential (indeed, *actual*)
chimp ancestors, as population B contains many human ancestors. Some
individuals in either population will end up having no living descendants,
but others will be the ancestor (if they're in population A) of every
chimpanzee alive today), or (if they're in population B) of every human
who's ever lived (and every Neanderthal, _Homo erectus_, australopith, and
so on). There is no one single mutant individual who is the sole ancestor
and cause of modern humans.
>
> Okay, so focusing now on the human ancestor population:
>
> Human ancestor population (24chrm)
> ______________________________ /??
>
> What happens at this point? A fusion occurs in a single individual in
> this population, supposedly, right? I take it that the proposed rare
> beneficial mutations do not hit several members of the population at
> the same time? Otherwise they wouldn't be rare.
>
There's no reason to suppose the change was beneficial, rather than neutral.
There's been speculation that the change in chromosomal numbers was linked
to the emergence of some distinctively human trait (e.g. bipedalism), but
there's no evidence for that that I'm aware of. Again, note that
differences in chromosome numbers seem to make no difference to okapis; it's
simply another way individuals in a population can vary.
Now, if you have a neutral mutation (one that makes an individual neither
more nor less fit in that particular environment), then its survival in each
generation is a matter of pure chance. Most neutral mutations presumably
die out in short order, swamped by the more common (even if no better)
alleles at that locus. But mathematical models show that, from time to
time, by sheer dumb luck, a neutral mutation will become more and more
common in each successive generation, until it completely replaces the
original trait.
http://www.talkorigins.org/faqs/genetic-drift.html
Humans and chimps have identical amino-acid sequences for the enzyme
cytochrome-c, but the *genes* for cytochrome-c differ in one nucleotide
between the two species (this is possible because there are multiple
three-nucleotide codons for each amino acid). This is a "silent" mutation
(one with no phenotypic effect), and surely neutral. It presumably
originated as a mutation in one individual in one species, and just by sheer
dumb luck spread through that species over hundreds of generations. This
can also happen to traits that do make a difference, if the difference
doesn't affect chances of reproductive success. Perhaps the spread of the
fused chromosome was just a case of neutral drift.
>
> Okay, so we now have a population of 24chrm members and one member's
> chromosomes 2a and 2b fuse into a single chromosome, forming
> chromosome 2 of the human ancestor's set of chromosomes.
>
> Supposedly, this 23chrm member of the 24chrm population can continue
> to interbreed with the 24chrm members, producing offspring that may or
> may not carry this 23chrm set. How does selection work in this case?
> Has it been demonstrated that Chromosome 2 in humans makes them
> distinctly different from apes, and gives them a distinct selective
> advantage? If not, it would be predicted that 23chrm members of the
> population would not necessarily increase but instead, as, they
> continue to interbreed, the 24chrm members will dominate because they
> are more in abundance, and the supposedly advantageous and distinct
> Chromosome 2 will die out and be lost to the population.
>
As noted, this happens most of the time, with most neutral mutations, but
every so often you get an exception. Flip enough coins enough times, and
sooner or later one will come up "heads" over and over and over.
>
> That would be one scenario. There's another. Looking at comparisons
> of human chromosome 2 and chimp chromosomes 2a and b, except for where
> the fusion supposedly occurs, the chromosomes appear to be physically
> identical. Problem here is which direction to go in giving value to
> the similarities.
>
> If the similarities mean that both human chromosome 2 and chimps
> chromosomes 2a and b will produce biological similarities, then what
> is there to choose from, selection wise, in order to give the
> advantage to Chromosome 2 in humans?
>
Maybe nothing. Not all evolution is the result of natural selection. And
there are problems with describing selection pressures on populations
millioins of years ago. There's a lot that isn't known about how genes
interact with each other and the environment to build an organism, and it's
hard to say what the effect would be. Even if we could say what the effect
would be, there's still the problem of figuring out why it would be
advantageous (there are several competing theories of why bipedalism, or
larger brains, or thinning body hair, would benefit our ancestors).
>
> But if, as research reveals (as recently as February, 2005),
> recombination hot spots on human chromosome 21, supposedly orthologous
> to chimp chromosome 22, are 83% different, and 17% similar -- then
> even though human Chromosome 2 and Chimp Chromosomes 2a and b appear
> to be almost identical, this apparent similarity may not be real after
> all.
>
> See:
>
This article discusses differences between human and chimp chromosomes in
where "crossovers" (e.g. the two copies of chromosome 22 switching parts
with each other) take place. I explained above why having 83% of genes
different is compatible with having 99% of DNA sequences identical. I don't
see any reference to "83%" in the article, but if it refers to "hotspots,"
rather than to genes or nucleotides, then I still don't see why this is
incompatible with either 99% sequence identity between genes, or with
virtually identical functions for genes. Presumably, the differences that
produce different "hotspots" are small, local changes in noncoding DNA
(which affect where the chromosome is likely to break apart during mating,
not how the genes themselves work), not in the genes themselves.
>
> http://www.admin.ox.ac.uk/po/050214.shtml
>
>>> Can you take it from there? What's the pathway? At this point, can
>>> the chimp ancestor still interbreed with either the common ancestor or
>>> with the human ancestor? It has to interbreed with something in order
>>> to produce more offspring after its own kind, so where does the
>>> partner come from?
>>>
>>Most evolutionists hold that most speciation events are "allopatric,"
>>meaning that they occur *after* the ancestral population has split into
>>two
>>groups that could interbreed if they met, but which no longer meet up.
>>Afterwards, mutation, genetic drift, and selection to different
>>environments
>>gradually change the populations into different species. No particular
>>mutation (unless you count polyploidy) is likely to produce a new species.
>>A better (though still oversimplified) approach would be to think of a
>>whole series of mutations, some beneficial, most neutral (but they still
>>made us different from chimps),
>
> no, no, no, you can't claim neutral mutations as changes that make us
> different from chimps. If humans become different, it would be
> because change (or mutation, as you call it) has occurred. No change,
> no difference. Neutral "mutations" cannot be counted to make a
> difference between humans and chimps. So once again you are left with
> trying to have the rare "beneficial" mutation carry the entire weight
> of your evolutionary theory.
>
Of course I can argue that. As noted above, some neutral changes are
"silent," with no phenotypic effect. But a change can produce a quite
marked effect, and still be "neutral" (that is, can make reproductive
success in the given environment neither more nor less likely). There are
two vireo (a type of bird) species that humans can easily tell apart only by
eye color. There's no reason to suppose that one eye color is better than
the other for the birds, but the difference distinguishes the two species.
Of course, the change might be beneficial in one population, because of
sexual selection (female fashion-consciousness), but that's not quite the
same thing as getting food more easily, avoiding becoming food, or fighting
off infections better. Quite possibly some of the differences between
humans and chimps were sexually rather than "naturally" selected.
As argued above, the change in chromosome number was quite possibly a
"neutral" change, although it is clearly one of the differences between us
and chimps. Note that something like 90% of the genome is neither genes nor
regulatory sequences. A lot of the 100 million or so differences between
the human and chimp genomes almost certainly don't make any difference that
matters to us -- they are "information" if you're looking for differences
between human and chimp genomes, but if you're looking for "what makes us
human," they aren't "information" in whatever sense it is that creationists
have in mind when they speak of "new information."
>
>> that each made the bearer a tiny bit more
>>"human" (or, in the other lineage, a tiny bit more "chimp"). No single
>>gene would have made its bearer much different from other members of his
>>species, or unable to interbreed with them.
>
> in which case, selection has nothing to work on, does it?
>
Again, mathematical models suggest that very small differences in "fitness"
can give a trait a big advantage over time. So, for that matter, do actual
observations of microevolution in the wild: Grant's finches on the Galapagos
had small differences in beak size and shape that hardly made them different
species, or even different subspecies -- but made a real difference in
fitness.
>
>>It doesn't seem likely that a modern human could (or at least would)
>>interbreed with a modern chimp, but presumably five million years ago, our
>>ancestors were just a tiny bit more "human" than the ancestors of modern
>>chimps.
>
> how can a life form be a tiny bit more human before it becomes human?
>
I said "human" in scare quotes. Maybe their brains were a trifle larger.
Maybe they walked erect a little more often and more easily. Maybe they
just had that silent mutation in the cytochrome-c gene (if a human had a
mutation that reversed that change, we wouldn't regard that person as less
human, of course, which is why I put "human" in scare quotes). The point
is, some of their evolutionary changes had made their genes (and probably,
if we looked closely enough, their bodies) a bit more like ours.
>
>> They probably could have produced fertile offspring with the chimp
>>ancestors, but as noted, they lived in different parts of Africa and no
>>longer met.
>
> I note the use of "probably" here.
>
Well, yes.
>
> snip>
>
-- Steven J.
John Harshman
No, that's not a principle, but we can't discard his first reason. It's
not just numbers of species but the shape of the phylogenetic tree that
determines what came first. Since we know the tree (i.e. that chimps,
gorillas, orangutans, and gibbons are successively less closely related
to humans), we know what came first. Either 24 pairs came first (and
humans evolved 23), or chimps, gorillas, orangutans, and gibbons all
evolved 24 pairs independently from an ancestor with 23 pairs. Which
makes more sense to you?
>>Second, while all
>>chromosomes have a centromere in the center and telomeres at the end, human
>>chromosome two has a vestigial centromere and telomere embedded in the
>>chromosome itself, suggesting that it was formed by a fusion of two
>>chromosomes. Indeed, there are two separate chromosomes in chimps that are
>>very similar in sequence to two "halves" of human chromosome 2.
>
> this would appear, on its surface, to be a more convincing reason to
> conclude that humans and chimps have a common ancestor (though you
> have not yet addressed how fusion affects fertility or the parallel
> meaning, if any, attached to chromosome fusion in mice.)
Parallel meaning? Fusion doesn't affect fertility very much, and in some
cases it doesn't affect it at all. How's that?
> That said, the latest evidence in genome comparison between chimps and
> humans reveal an 83% difference between chimp chromosome 22 and human
> chromosome 21 (chimp chromosome 22 is said to be the ortholog of human
> chromosome 21.)
I'm afraid you will have to tell us where you got that number, and what
it means. You have misunderstood something seriously, but I don't know
what. Ah, looking below I find you do tell us. The 83% difference is in
the location of recombination hot spots, not sequence. This would be a
very silly measure of genetic difference. In fact, as the press release
says, it doesn't seem to involve genetic differences at all. The DNA
sequence itself is still 99% identical.
> And even though there appears to be 99% similarity
> between the DNA of humans and chimps, the recombination hot spots have
> turned out to be almost completely different. Apparently, then, DNA
> sequences, even though highly similar, do not determine biological
> function.
Now that's a bundle of non sequiturs. Explain what you think you mean by
that. Of course they determine biological function. What they apparently
don't do is determine the sites at which recombination happens. That's
one biological function, not "biological function".
> It's like comparing the recipes for two cakes. They both use 99%
> similar ingredients -- flour, sugar, butter, eggs. Does this
> similarity mean that both cakes came from the same batter? Not
> necessarily. Not even probably. The more reasonable assumption is
> that both cakes were created in their own right, from different
> recipes, but using similar ingredients.
This analogy has nothing at all to do with the similarity of DNA.
Further, the major evidence for common descent is not mere similarity,
but (have you heard this before?) nested hierarchy. Cakes just don't
display any such thing.
>>By the way, although you didn't explicitly ask, the okapi (a rare,
>>short-necked giraffe) species has individuals with 22 pairs of chromosomes,
>>23 pairs, and even 22.5 pairs (for 45 chromosomes in all -- in which case
>>two chromosomes from one parent must be paired with one -- fused --
>>chromosome from the other parent).
>
> would you have references, by any chance, to studies that have
> followed the interbreeding of these subspecies of opaki? Have they
> tried to interbreed an opaki with 22 pairs of chromosomes with an
> opaki that has 23 pairs of chromosomes? Or do opakis with 22 pairs of
> chromosomes breed only with those that have 22 pairs of chromosomes,
> and so on?
>
>> So a mutation that produced the first
>>human with a chromosome 2 (rather than the ancestral chromosomes 2a and 2b)
>>would not have prevented that individual from mating successfully.
>
> I'm not sure that that is a hard-and-fast conclusion, considering that
> there is no evidence today that humans with chromosome 2 can
> interbreed with chimps with chromosomes 2a and 2b. If they can't
> today, why speculate that they could have at one time, unless you have
> evidence that such a thing is possible?
Check out the mice, the shrews, and other species in which chromosomal
fusions are within-population polymorphisms.
>>Or, take
>>the case of Przewalski's horse and the domestic horse: domestic horses, like
>>their human breeders, have one fewer chromosome pairs than their wild
>>ancestors, due, apparently, to a chromosomal fusion -- but domestic and
>>Przewalski's horses can still interbreed to produce fertile offspring. In
>>other cases (e.g. "chromosomal races" of mice), having different chromosome
>>numbers reduces interfertility.
>
> if you are comparing the horse scenario to the human/chimp scenario,
> you would need to explain why the domestic horse can still breed
> successfully with their wild ancestor, the Przewalski horse, and yet
> humans cannot breed with their supposed wild ancestor, the ape.
Przewalski's horse is not the ancestor of domestic horses. It's a close
relative. The factors that allow or prevent interbreeding are complex,
but simple length of time apart is one of them. Humans and chimps have
been separated longer than the two horse species. Morphological
divergence is another, and we have diverged more than the horses.
You are still having problems with ASCII graphics, assuming this is
supposed to be a tree.
> Chimp ancestor population (24chrm)
> common ancestor (24 chrm) /_____________________
> ___________________________/
> \
> \
> Human ancestor population (24chrm)
>
> At this point, there is as yet no change in the genetic makeup of
> either the chimp ancestor population or the human ancestor population.
> The only change is in geographical location which prevents Population
> A (containing a potential chimp ancestor) from interbreeding with
> Population B (containing a potential human ancestor).
>
> Right so far?
>
> Okay, so focusing now on the human ancestor population:
>
> Human ancestor population (24chrm)
> ______________________________ /??
>
> What happens at this point? A fusion occurs in a single individual in
> this population, supposedly, right? I take it that the proposed rare
> beneficial mutations do not hit several members of the population at
> the same time? Otherwise they wouldn't be rare.
Right. But nobody says this fusion is beneficial, and nobody says it's
the first difference to become fixed in the human lineage.
> Okay, so we now have a population of 24chrm members and one member's
> chromosomes 2a and 2b fuse into a single chromosome, forming
> chromosome 2 of the human ancestor's set of chromosomes.
>
> Supposedly, this 23chrm member of the 24chrm population can continue
> to interbreed with the 24chrm members, producing offspring that may or
> may not carry this 23chrm set. How does selection work in this case?
> Has it been demonstrated that Chromosome 2 in humans makes them
> distinctly different from apes, and gives them a distinct selective
> advantage?
No. There's no reason to suppose it does.
> If not, it would be predicted that 23chrm members of the
> population would not necessarily increase but instead, as, they
> continue to interbreed, the 24chrm members will dominate because they
> are more in abundance, and the supposedly advantageous and distinct
> Chromosome 2 will die out and be lost to the population.
You need to read up on genetic drift. Chromosomal mutations happen with
a certain frequency. Most are lost. By chance, a few increase in
frequency and eventually become fixed. This could easily be such a case.
> That would be one scenario. There's another. Looking at comparisons
> of human chromosome 2 and chimp chromosomes 2a and b, except for where
> the fusion supposedly occurs, the chromosomes appear to be physically
> identical. Problem here is which direction to go in giving value to
> the similarities.
>
> If the similarities mean that both human chromosome 2 and chimps
> chromosomes 2a and b will produce biological similarities, then what
> is there to choose from, selection wise, in order to give the
> advantage to Chromosome 2 in humans?
>
> But if, as research reveals (as recently as February, 2005),
> recombination hot spots on human chromosome 21, supposedly orthologous
> to chimp chromosome 22, are 83% different, and 17% similar -- then
> even though human Chromosome 2 and Chimp Chromosomes 2a and b appear
> to be almost identical, this apparent similarity may not be real after
> all.
>
> See:
>
> http://www.admin.ox.ac.uk/po/050214.shtml
I really don't understand why you take this the way you do. As the press
release says, this doesn't mean the genomes are different. It means that
the location of recombination is under the control of some mechanism
that doesn't depend on the DNA sequence at that location. The DNA is
still 99% identical.
>>>Can you take it from there? What's the pathway? At this point, can
>>>the chimp ancestor still interbreed with either the common ancestor or
>>>with the human ancestor? It has to interbreed with something in order
>>>to produce more offspring after its own kind, so where does the
>>>partner come from?
>>>
>>
>>Most evolutionists hold that most speciation events are "allopatric,"
>>meaning that they occur *after* the ancestral population has split into two
>>groups that could interbreed if they met, but which no longer meet up.
>>Afterwards, mutation, genetic drift, and selection to different environments
>>gradually change the populations into different species. No particular
>>mutation (unless you count polyploidy) is likely to produce a new species.
>>A better (though still oversimplified) approach would be to think of a
>>whole series of mutations, some beneficial, most neutral (but they still
>>made us different from chimps),
>
> no, no, no, you can't claim neutral mutations as changes that make us
> different from chimps. If humans become different, it would be
> because change (or mutation, as you call it) has occurred. No change,
> no difference. Neutral "mutations" cannot be counted to make a
> difference between humans and chimps. So once again you are left with
> trying to have the rare "beneficial" mutation carry the entire weight
> of your evolutionary theory.
This depends on what you mean by "different". If you're talking about
that 1% difference in DNA sequence, then most of it is due to neutral
mutations. If you're talking about the differences in morphology, well
of course most of those neutral mutations have nothing to do with that,
and it must be the relatively few beneficial mutations that are mostly
responsible. (I'm hedging here because it's entirely possible for a
mutation with a phenotypic effect to be neutral too.)
>>that each made the bearer a tiny bit more
>>"human" (or, in the other lineage, a tiny bit more "chimp"). No single
>>gene would have made its bearer much different from other members of his
>>species, or unable to interbreed with them.
>
> in which case, selection has nothing to work on, does it?
Wrong. Selection works on individual variation within species, and it
can easily work on small differences. Big changes cana result from the
accumulation over time of little changes.
>>It doesn't seem likely that a modern human could (or at least would)
>>interbreed with a modern chimp, but presumably five million years ago, our
>>ancestors were just a tiny bit more "human" than the ancestors of modern
>>chimps.
>
>
> how can a life form be a tiny bit more human before it becomes human?
How can it not? I don't understand your objection here. We're talking
about intermediates. Do you deny even the logical possibility of
intermediate forms?
>> They probably could have produced fertile offspring with the chimp
>>ancestors, but as noted, they lived in different parts of Africa and no
>>longer met.
>
>
> I note the use of "probably" here.
Yes. That's because we don't know, and have no way of ever knowing,
exactly when reproductive isolatio evolved between the two lineages.
Zoe
<sjt195...@nts.link.net.INVALID> wrote:
I see. I suppose that's a good speculative answer but not
sufficiently scientific to hang an evolutionary cap upon. Call it a
neutral position -- makes no difference one way or the other.
see:
http://genomebiology.com/researchnews/default.asp?arx_id=gb-spotlight-20040528-01
Begin quote:
'Sakaki said their analysis found about 68,000 insertions or
deletions. "That is almost one insertion/deletion every 470 bases," he
said. In addition, a small proportion of genes showed a relatively
higher rate of evolution than most other genes. "We haven't known what
proportion of the genes shows adaptive evolution. This study shows it
to be about 2 to 3%," he said.
'Early molecular comparisons between humans and chimpanzees suggested
that the species are very similar to each other at the nucleotide
sequence level - a difference of between 1.23% and 5%, Sakaki said.
The results reported this week showed that "83% of the genes have
changed between the human and the chimpanzee - only 17% are identical
- so that means that the impression that comes from the 1.2%
[sequence] difference is [misleading]. In the case of protein
structures, it has a big effect," Sakaki said.'
End quote.
I recognize that this is written from an evolutionary point of view,
so expect to find attempts to explain the differences in terms of
change and loss or gain. But, really now, if a difference between the
two is observed, there is nothing to say that the present difference
is a result of change over millions of years, or if the difference was
present from the time of origin.
Further in the article, Derek Wildman tries to hold onto the idea that
similarity must still mean relationship through a common ancestor, but
I'm betting that with further comparison between the chimp genome and
the human genome, this idea of relationship through a common ancestor
will continue to degrade.
> Suppose (these figures are illustrative only; do not
>assume they reflect actual measurements of the chromosome) that two
>chromosomes in different species have 100 genes each. Suppose each gene has
>300 nucleotides, and that for each gene two nucleotides differ between the
>two species. That would mean that on this chromosome, 100% of the genes are
>(slightly) different from their homologues in the other species, but that
>overall sequence similarity is over 99%.
Quoting further from the above link:
'Early molecular comparisons between humans and chimpanzees suggested
that the species are very similar to each other at the nucleotide
sequence level - a difference of between 1.23% and 5%, Sakaki said.
The results reported this week showed that "83% of the genes have
changed between the human and the chimpanzee - only 17% are identical
- so that means that the impression that comes from the 1.2%
[sequence] difference is [misleading]. In the case of protein
structures, it has a big effect," Sakaki said.'
End quote.
> But certainly minor differences in
>DNA sequence can produce major changes in function, and certainly genes by
>themselves do not determine everything that happens in an organism.
what are some other things, besides changes in genes, that are
suggested would cause the kind of changes in an organism that would
lead its population in a direction away from its old genus to a new
one?
>> It's like comparing the recipes for two cakes. They both use 99%
>> similar ingredients -- flour, sugar, butter, eggs. Does this
>> similarity mean that both cakes came from the same batter? Not
>> necessarily. Not even probably. The more reasonable assumption is
>> that both cakes were created in their own right, from different
>> recipes, but using similar ingredients.
>>
>Actually, a sufficient similarity in composition (exact proportions of many
>minor ingredients) may strongly indicate origin from the same batter. At
>least, this line of reasoning is commonly used in forensic science for
>bullet fragments and dirt samples.
we do not have access to exact proportions in biology. In forensic
science, there is access to the original firearm and the original
source of dirt for comparison purposes. Not so in biology.
> But in any case, a closer analogy to DNA
>would be the exact wording of the recipes themselves -- especially if both
>recipes shared the same mispellings of the same words in the same order, and
>had bits of text that were alike but didn't seem to have anything to do with
>the actual recipe (like, e.g. the pseudogenes and endogenous retroviruses
>chimps and humans share).
recipes aren't available biologically so the analogy falls apart at
this point.
But, again, similarity is not sufficient to indicate relationship
through a common ancestor, as is being seen in in the latest
chimp/human genome comparisons.
>By the way, why is it more reasonable, even if we don't know for sure, to
>suppose that the cakes were created from different recipes and different
>batter?
because, from experience, we know that cakes come from different
batters. There is not one single grand clearing house of cake batter
from which all cakes come.
> Certainly a baker is capable of making one big batch of batter and
>making lots of cakes from it.
yes, but there is no single common source of batter to all cakes.
> And a Creator, I would suppose, is perfectly
>capable of making many species from a single ancestral population, as He
>made (according to the Bible) many nations from one original human
>population.
but we don't think that cakes and cars come from the same batter or
assembly line, do we? There is no one common source of material to
all categories of things, just as there is no one common ancestor to
all categories of life forms.
>>>By the way, although you didn't explicitly ask, the okapi (a rare,
>>>short-necked giraffe) species has individuals with 22 pairs of
>>>chromosomes,
>>>23 pairs, and even 22.5 pairs (for 45 chromosomes in all -- in which case
>>>two chromosomes from one parent must be paired with one -- fused --
>>>chromosome from the other parent).
>>
>> would you have references, by any chance, to studies that have
>> followed the interbreeding of these subspecies of opaki? Have they
>> tried to interbreed an opaki with 22 pairs of chromosomes with an
>> opaki that has 23 pairs of chromosomes? Or do opakis with 22 pairs of
>> chromosomes breed only with those that have 22 pairs of chromosomes,
>> and so on?
>>
>Okapis have no known subspecies; the variant chromosome numbers do not
>correspond to racial or habitat differences. And, apparently, they
>interbreed freely with okapis with different numbers of chromosomes and
>produce fertile offspring. Google turns up a few scholarly articles on
>"chromosomal polymorphism" in okapis and other species, and this appears, in
>okapis and some other species, to work like any other polymorphism (that is,
>it no more affects interbreeding than the difference between, say, type A
>and type O blood, or blue and brown eyes).
so these scholarly articles to which you refer, do they mention having
tested the chromosomes of known parents to known offspring and having
discovered that the chromosome counts differ in the parents? Or is
the testing randomly done, without checking to see if those opaki with
same chromosome counts might tend to be attracted to each other, or
whether different chromosome-count opakis tend to repel each other?
>>> So a mutation that produced the first
>>>human with a chromosome 2 (rather than the ancestral chromosomes 2a and
>>>2b)
>>>would not have prevented that individual from mating successfully.
>>
>> I'm not sure that that is a hard-and-fast conclusion, considering that
>> there is no evidence today that humans with chromosome 2 can
>> interbreed with chimps with chromosomes 2a and 2b. If they can't
>> today, why speculate that they could have at one time, unless you have
>> evidence that such a thing is possible?
>>
>There's no evidence that chimps with chromosomes 2a and 2b can interbreed
>with gorillas with chromosomes 2a and 2b. They've spent seven million years
>or more evolving in different directions (not just in obvious anatomical
>ways, but in more subtle ones). For all either of us knows, hominins (the
>human side of the human-chimp lineage) and panins (the chimp side) stopped
>being interfertile before the chromosome fusion happened in the hominin
>line. I doubt that chromosome number per se is much of a guide to
>interfertility.
so it's just guesswork here at this point?
>But again, horse subspecies with different numbers of chromosomes are
>interfertile. Okapis with a rather recent mutation that produced a fused
>chromosome are interfertile. I'm speculating that what is known to happen
>in several species today could have happened in other species at other
>times; it seems a safe enough speculation.
okay, it's still speculation. Moving on...
okay.
so are you saying that many members of Population B got hit by the
same rare benefit mutation, or are you saying that many members of
Population B result from a single member getting hit by the rare
beneficial mutation and passing it down to offspring?
And I take it that Population A must have been hit with some other
kind of rare beneficial mutation in order for it to begin to exhibit
characteristics of chimpness?
> Some
>individuals in either population will end up having no living descendants,
>but others will be the ancestor (if they're in population A) of every
>chimpanzee alive today), or (if they're in population B) of every human
>who's ever lived (and every Neanderthal, _Homo erectus_, australopith, and
>so on). There is no one single mutant individual who is the sole ancestor
>and cause of modern humans.
well, it has got to start with a single member, unless you are
proposing that the same rare beneficial mutation hits many members of
the population at the same time or within a certain time frame?
>> Okay, so focusing now on the human ancestor population:
>>
>> Human ancestor population (24chrm)
>> ______________________________ /??
>>
>> What happens at this point? A fusion occurs in a single individual in
>> this population, supposedly, right? I take it that the proposed rare
>> beneficial mutations do not hit several members of the population at
>> the same time? Otherwise they wouldn't be rare.
>>
>There's no reason to suppose the change was beneficial, rather than neutral.
it has to be beneficial, according to your theory, in order to get
selected. If it's neutral, there's nothing to select.
>There's been speculation that the change in chromosomal numbers was linked
>to the emergence of some distinctively human trait (e.g. bipedalism), but
>there's no evidence for that that I'm aware of. Again, note that
>differences in chromosome numbers seem to make no difference to okapis; it's
>simply another way individuals in a population can vary.
>
>Now, if you have a neutral mutation (one that makes an individual neither
>more nor less fit in that particular environment), then its survival in each
>generation is a matter of pure chance. Most neutral mutations presumably
>die out in short order, swamped by the more common (even if no better)
>alleles at that locus. But mathematical models show that, from time to
>time, by sheer dumb luck, a neutral mutation will become more and more
>common in each successive generation, until it completely replaces the
>original trait.
so the entire evolutionary framework consists of sheer dumb luck. Not
very scientific or predictable, is it?
>http://www.talkorigins.org/faqs/genetic-drift.html
>
>Humans and chimps have identical amino-acid sequences for the enzyme
>cytochrome-c, but the *genes* for cytochrome-c differ in one nucleotide
>between the two species (this is possible because there are multiple
>three-nucleotide codons for each amino acid). This is a "silent" mutation
>(one with no phenotypic effect), and surely neutral. It presumably
>originated as a mutation in one individual in one species, and just by sheer
>dumb luck spread through that species over hundreds of generations. This
>can also happen to traits that do make a difference, if the difference
>doesn't affect chances of reproductive success. Perhaps the spread of the
>fused chromosome was just a case of neutral drift.
"presumably" "perhaps" "speculated" "sheer dumb luck" "seem to"
"there's no evidence" "pure chance" -- sorry, Steven, but none of this
sounds very scientific. And these terms are used in connection with
the central core of your theory. How is this expected to command
respect from any thinking but undecided person? Gravity, which many
like to have placed in the same category as evolutionary theory, does
not consist of a series of maybes and perhapses.
>> Okay, so we now have a population of 24chrm members and one member's
>> chromosomes 2a and 2b fuse into a single chromosome, forming
>> chromosome 2 of the human ancestor's set of chromosomes.
>>
>> Supposedly, this 23chrm member of the 24chrm population can continue
>> to interbreed with the 24chrm members, producing offspring that may or
>> may not carry this 23chrm set. How does selection work in this case?
>> Has it been demonstrated that Chromosome 2 in humans makes them
>> distinctly different from apes, and gives them a distinct selective
>> advantage? If not, it would be predicted that 23chrm members of the
>> population would not necessarily increase but instead, as, they
>> continue to interbreed, the 24chrm members will dominate because they
>> are more in abundance, and the supposedly advantageous and distinct
>> Chromosome 2 will die out and be lost to the population.
>>
>As noted, this happens most of the time, with most neutral mutations, but
>every so often you get an exception. Flip enough coins enough times, and
>sooner or later one will come up "heads" over and over and over.
your whole theory is built upon the flip of the coin. Still not a
scientific approach.
>> That would be one scenario. There's another. Looking at comparisons
>> of human chromosome 2 and chimp chromosomes 2a and b, except for where
>> the fusion supposedly occurs, the chromosomes appear to be physically
>> identical. Problem here is which direction to go in giving value to
>> the similarities.
>>
>> If the similarities mean that both human chromosome 2 and chimps
>> chromosomes 2a and b will produce biological similarities, then what
>> is there to choose from, selection wise, in order to give the
>> advantage to Chromosome 2 in humans?
>>
>Maybe nothing. Not all evolution is the result of natural selection.
but natural selection is a biggie, isn't it? What's left?
> And
>there are problems with describing selection pressures on populations
>millioins of years ago.
of course there are. So why the strident, dogmatic stance of so many
posters on TO -- excluding you, of course.
> There's a lot that isn't known about how genes
>interact with each other and the environment to build an organism, and it's
>hard to say what the effect would be. Even if we could say what the effect
>would be, there's still the problem of figuring out why it would be
>advantageous (there are several competing theories of why bipedalism, or
>larger brains, or thinning body hair, would benefit our ancestors).
thank you for a fair and impartial answer.
>> But if, as research reveals (as recently as February, 2005),
>> recombination hot spots on human chromosome 21, supposedly orthologous
>> to chimp chromosome 22, are 83% different, and 17% similar -- then
>> even though human Chromosome 2 and Chimp Chromosomes 2a and b appear
>> to be almost identical, this apparent similarity may not be real after
>> all.
>>
>> See:
>>
>This article discusses differences between human and chimp chromosomes in
>where "crossovers" (e.g. the two copies of chromosome 22 switching parts
>with each other) take place. I explained above why having 83% of genes
>different is compatible with having 99% of DNA sequences identical. I don't
>see any reference to "83%" in the article, but if it refers to "hotspots,"
>rather than to genes or nucleotides, then I still don't see why this is
>incompatible with either 99% sequence identity between genes, or with
>virtually identical functions for genes. Presumably, the differences that
>produce different "hotspots" are small, local changes in noncoding DNA
>(which affect where the chromosome is likely to break apart during mating,
>not how the genes themselves work), not in the genes themselves.
see the link above.
and selection works with phenotypic effect, I take it?
> But a change can produce a quite
>marked effect, and still be "neutral" (that is, can make reproductive
>success in the given environment neither more nor less likely).
I didn't think that is what was meant by neutral mutations. There are
two definitions that I see so far, used by evolutionists:
1) A mutation that has no effect on the Darwinian fitness of its
carriers.
2) A mutation that has no phenotypic effect.
Where is the "marked effect" in the above understanding of neutral
mutations?
> There are
>two vireo (a type of bird) species that humans can easily tell apart only by
>eye color. There's no reason to suppose that one eye color is better than
>the other for the birds, but the difference distinguishes the two species.
wait a minute. Does difference in eye color alone make a new species?
Then a blue-eyed human is a different species from a brown-eyed human?
>Of course, the change might be beneficial in one population, because of
>sexual selection (female fashion-consciousness), but that's not quite the
>same thing as getting food more easily, avoiding becoming food, or fighting
>off infections better. Quite possibly some of the differences between
>humans and chimps were sexually rather than "naturally" selected.
add "quite possibly" to the dictionary of evolutionary theory. So far
nothing scientific. What is scientific is the actual data. The
theory proposed in regard to the data, however, being based on maybes
and possiblies, is not scientific.
>As argued above, the change in chromosome number was quite possibly a
>"neutral" change, although it is clearly one of the differences between us
>and chimps. Note that something like 90% of the genome is neither genes nor
>regulatory sequences.
it would be expected that more than 90% of a cell's chromosomes (the
genome) would have its genes turned off and unrecognizable as genes
since only 3% or so of each cell's chromosomes have genes turned on to
code for the protein making of that particular cell type. This does
not mean that the noncoding material is junk. It just is not used for
that particular cell's purpose. And I would expect that when not
actively in use, the potential for gene formation sits around looking
for all the world like junk.
> A lot of the 100 million or so differences between
>the human and chimp genomes almost certainly don't make any difference that
>matters to us -- they are "information" if you're looking for differences
>between human and chimp genomes, but if you're looking for "what makes us
>human," they aren't "information" in whatever sense it is that creationists
>have in mind when they speak of "new information."
I'm not following you here.
>>> that each made the bearer a tiny bit more
>>>"human" (or, in the other lineage, a tiny bit more "chimp"). No single
>>>gene would have made its bearer much different from other members of his
>>>species, or unable to interbreed with them.
>>
>> in which case, selection has nothing to work on, does it?
>>
>Again, mathematical models suggest that very small differences in "fitness"
>can give a trait a big advantage over time.
"small differences" aren't the same as neutral differences, are they?
> So, for that matter, do actual
>observations of microevolution in the wild: Grant's finches on the Galapagos
>had small differences in beak size and shape that hardly made them different
>species, or even different subspecies -- but made a real difference in
>fitness.
>>
>>>It doesn't seem likely that a modern human could (or at least would)
>>>interbreed with a modern chimp, but presumably five million years ago, our
>>>ancestors were just a tiny bit more "human" than the ancestors of modern
>>>chimps.
>>
>> how can a life form be a tiny bit more human before it becomes human?
>>
>I said "human" in scare quotes. Maybe their brains were a trifle larger.
>Maybe they walked erect a little more often and more easily. Maybe they
>just had that silent mutation in the cytochrome-c gene (if a human had a
>mutation that reversed that change, we wouldn't regard that person as less
>human, of course, which is why I put "human" in scare quotes). The point
>is, some of their evolutionary changes had made their genes (and probably,
>if we looked closely enough, their bodies) a bit more like ours.
add "maybe" and scare quotes to the lexicon.
>>> They probably could have produced fertile offspring with the chimp
>>>ancestors, but as noted, they lived in different parts of Africa and no
>>>longer met.
>>
>> I note the use of "probably" here.
>>
>Well, yes.
thank you.
Zoe
the shape of the phylogenetic tree is a subjective one, based on the
subjective opinions of the taxonomist and cladist, right?
> Since we know the tree (i.e. that chimps,
>gorillas, orangutans, and gibbons are successively less closely related
>to humans),
isn't this what is called assuming your conclusion? You say,
authoritatively, We know that these creatures are successively less
closely related to humans. How do we know this? By our phylogenetic
tree that we have subjectively made up.
> we know what came first. Either 24 pairs came first (and
>humans evolved 23), or chimps, gorillas, orangutans, and gibbons all
>evolved 24 pairs independently from an ancestor with 23 pairs. Which
>makes more sense to you?
if I were forced to embrace evolutionary theory, I would have to say
that fusion makes more sense than fission. But fission is just as
plausible within the evolutionary framework in which many life forms
emerge from a single common ancestor.
>
>>>Second, while all
>>>chromosomes have a centromere in the center and telomeres at the end, human
>>>chromosome two has a vestigial centromere and telomere embedded in the
>>>chromosome itself, suggesting that it was formed by a fusion of two
>>>chromosomes. Indeed, there are two separate chromosomes in chimps that are
>>>very similar in sequence to two "halves" of human chromosome 2.
>>
>> this would appear, on its surface, to be a more convincing reason to
>> conclude that humans and chimps have a common ancestor (though you
>> have not yet addressed how fusion affects fertility or the parallel
>> meaning, if any, attached to chromosome fusion in mice.)
>
>Parallel meaning?
if chromosome fusion is used as evidence of a split from a common
ancestor population, does chromosome fusion in mice also represent a
split from a common ancestor population, especially as mice and humans
are almost identical in their genetic makeup, as well?
>Fusion doesn't affect fertility very much, and in some
>cases it doesn't affect it at all. How's that?
too vague.
>> That said, the latest evidence in genome comparison between chimps and
>> humans reveal an 83% difference between chimp chromosome 22 and human
>> chromosome 21 (chimp chromosome 22 is said to be the ortholog of human
>> chromosome 21.)
>
>I'm afraid you will have to tell us where you got that number, and what
>it means. You have misunderstood something seriously, but I don't know
>what. Ah, looking below I find you do tell us. The 83% difference is in
>the location of recombination hot spots, not sequence. This would be a
>very silly measure of genetic difference. In fact, as the press release
>says, it doesn't seem to involve genetic differences at all. The DNA
>sequence itself is still 99% identical.
See:
http://genomebiology.com/researchnews/default.asp?arx_id=gb-spotlight-20040528-01
>> And even though there appears to be 99% similarity
>> between the DNA of humans and chimps, the recombination hot spots have
>> turned out to be almost completely different. Apparently, then, DNA
>> sequences, even though highly similar, do not determine biological
>> function.
>
>Now that's a bundle of non sequiturs. Explain what you think you mean by
>that. Of course they determine biological function. What they apparently
>don't do is determine the sites at which recombination happens. That's
>one biological function, not "biological function".
bring this up again AFTER reading the above link.
>> It's like comparing the recipes for two cakes. They both use 99%
>> similar ingredients -- flour, sugar, butter, eggs. Does this
>> similarity mean that both cakes came from the same batter? Not
>> necessarily. Not even probably. The more reasonable assumption is
>> that both cakes were created in their own right, from different
>> recipes, but using similar ingredients.
>
>This analogy has nothing at all to do with the similarity of DNA.
>Further, the major evidence for common descent is not mere similarity,
>but (have you heard this before?) nested hierarchy. Cakes just don't
>display any such thing.
every analogy breaks down sooner or later.
>>>By the way, although you didn't explicitly ask, the okapi (a rare,
>>>short-necked giraffe) species has individuals with 22 pairs of chromosomes,
>>>23 pairs, and even 22.5 pairs (for 45 chromosomes in all -- in which case
>>>two chromosomes from one parent must be paired with one -- fused --
>>>chromosome from the other parent).
>>
>> would you have references, by any chance, to studies that have
>> followed the interbreeding of these subspecies of opaki? Have they
>> tried to interbreed an opaki with 22 pairs of chromosomes with an
>> opaki that has 23 pairs of chromosomes? Or do opakis with 22 pairs of
>> chromosomes breed only with those that have 22 pairs of chromosomes,
>> and so on?
>>
>>> So a mutation that produced the first
>>>human with a chromosome 2 (rather than the ancestral chromosomes 2a and 2b)
>>>would not have prevented that individual from mating successfully.
>>
>> I'm not sure that that is a hard-and-fast conclusion, considering that
>> there is no evidence today that humans with chromosome 2 can
>> interbreed with chimps with chromosomes 2a and 2b. If they can't
>> today, why speculate that they could have at one time, unless you have
>> evidence that such a thing is possible?
>
>Check out the mice, the shrews, and other species in which chromosomal
>fusions are within-population polymorphisms.
have they checked the parents of particular offspring and found that
different-numbered genomes were able to interbreed? Or did they
simply test various members, found that some have a certain number
chromosome count, and others a different count, and assumed that
different counts could interbreed?
>>>Or, take
>>>the case of Przewalski's horse and the domestic horse: domestic horses, like
>>>their human breeders, have one fewer chromosome pairs than their wild
>>>ancestors, due, apparently, to a chromosomal fusion -- but domestic and
>>>Przewalski's horses can still interbreed to produce fertile offspring. In
>>>other cases (e.g. "chromosomal races" of mice), having different chromosome
>>>numbers reduces interfertility.
>>
>> if you are comparing the horse scenario to the human/chimp scenario,
>> you would need to explain why the domestic horse can still breed
>> successfully with their wild ancestor, the Przewalski horse, and yet
>> humans cannot breed with their supposed wild ancestor, the ape.
>
>Przewalski's horse is not the ancestor of domestic horses. It's a close
>relative.
well, Steven called it "ancestors." Could you and he come to some
agreement?
>The factors that allow or prevent interbreeding are complex,
>but simple length of time apart is one of them.
so would your theory predict that the Chinese race, living apart from
the Indian race, would eventually, over time, evolve the inability to
interbreed?
no, this is not a tree. This is the beginning of what could be a
tree. I'm waiting for you to tell me how this tree grows.
>
>> Chimp ancestor population (24chrm)
>> common ancestor (24 chrm) /_____________________
>> ___________________________/
>> \
>> \
>> Human ancestor population (24chrm)
>>
>> At this point, there is as yet no change in the genetic makeup of
>> either the chimp ancestor population or the human ancestor population.
>> The only change is in geographical location which prevents Population
>> A (containing a potential chimp ancestor) from interbreeding with
>> Population B (containing a potential human ancestor).
>>
>> Right so far?
>>
>> Okay, so focusing now on the human ancestor population:
>>
>> Human ancestor population (24chrm)
>> ______________________________ /??
>>
>> What happens at this point? A fusion occurs in a single individual in
>> this population, supposedly, right? I take it that the proposed rare
>> beneficial mutations do not hit several members of the population at
>> the same time? Otherwise they wouldn't be rare.
>
>Right. But nobody says this fusion is beneficial, and nobody says it's
>the first difference to become fixed in the human lineage.
so now evolutionary theory proposes that life forms evolve, not only
from selected beneficial mutations, but from harmful and/or neutral
mutations?
>> Okay, so we now have a population of 24chrm members and one member's
>> chromosomes 2a and 2b fuse into a single chromosome, forming
>> chromosome 2 of the human ancestor's set of chromosomes.
>>
>> Supposedly, this 23chrm member of the 24chrm population can continue
>> to interbreed with the 24chrm members, producing offspring that may or
>> may not carry this 23chrm set. How does selection work in this case?
>> Has it been demonstrated that Chromosome 2 in humans makes them
>> distinctly different from apes, and gives them a distinct selective
>> advantage?
>
>No. There's no reason to suppose it does.
so how does your mechanism of selected beneficial mutation work then?
If chromosome2 is the main piece of evidence that chimps and humans
come from a common ancestor, and yet this piece of evidence makes no
difference in the life form containing the fusion, what is there to
select?
>> If not, it would be predicted that 23chrm members of the
>> population would not necessarily increase but instead, as, they
>> continue to interbreed, the 24chrm members will dominate because they
>> are more in abundance, and the supposedly advantageous and distinct
>> Chromosome 2 will die out and be lost to the population.
>
>You need to read up on genetic drift. Chromosomal mutations happen with
>a certain frequency. Most are lost. By chance, a few increase in
>frequency and eventually become fixed. This could easily be such a case.
saying so doesn't make it so. Where's Deadrat when I need him. Maybe
he could draw up a mathematical formula that will demonstrate how
chance "beneficial" mutations that make no difference can get selected
for.
snip>
>>>It doesn't seem likely that a modern human could (or at least would)
>>>interbreed with a modern chimp, but presumably five million years ago, our
>>>ancestors were just a tiny bit more "human" than the ancestors of modern
>>>chimps.
>>
>>
>> how can a life form be a tiny bit more human before it becomes human?
>
>How can it not? I don't understand your objection here. We're talking
>about intermediates. Do you deny even the logical possibility of
>intermediate forms?
intermediate forms between an apple and a carrot? No. Intermediate
forms between a carrot and a snail? No. Intermediate forms between
a dinosaur and a bird? No.
>>> They probably could have produced fertile offspring with the chimp
>>>ancestors, but as noted, they lived in different parts of Africa and no
>>>longer met.
>>
>>
>> I note the use of "probably" here.
>
>Yes. That's because we don't know, and have no way of ever knowing,
>exactly when reproductive isolatio evolved between the two lineages.
I'm not asking for when it happened, but how it happened. So far, no
steps have been given other than probabilities and maybes.
John Harshman
No. You have been told about this before, but you never seem to listen.
>>Since we know the tree (i.e. that chimps,
>>gorillas, orangutans, and gibbons are successively less closely related
>>to humans),
>
> isn't this what is called assuming your conclusion? You say,
> authoritatively, We know that these creatures are successively less
> closely related to humans. How do we know this? By our phylogenetic
> tree that we have subjectively made up.
It's not subjective. We've been over this before.
>>we know what came first. Either 24 pairs came first (and
>>humans evolved 23), or chimps, gorillas, orangutans, and gibbons all
>>evolved 24 pairs independently from an ancestor with 23 pairs. Which
>>makes more sense to you?
>
> if I were forced to embrace evolutionary theory, I would have to say
> that fusion makes more sense than fission. But fission is just as
> plausible within the evolutionary framework in which many life forms
> emerge from a single common ancestor.
That makes no sense.
>>>>Second, while all
>>>>chromosomes have a centromere in the center and telomeres at the end, human
>>>>chromosome two has a vestigial centromere and telomere embedded in the
>>>>chromosome itself, suggesting that it was formed by a fusion of two
>>>>chromosomes. Indeed, there are two separate chromosomes in chimps that are
>>>>very similar in sequence to two "halves" of human chromosome 2.
>>>
>>>this would appear, on its surface, to be a more convincing reason to
>>>conclude that humans and chimps have a common ancestor (though you
>>>have not yet addressed how fusion affects fertility or the parallel
>>>meaning, if any, attached to chromosome fusion in mice.)
>>
>>Parallel meaning?
>
> if chromosome fusion is used as evidence of a split from a common
> ancestor population, does chromosome fusion in mice also represent a
> split from a common ancestor population, especially as mice and humans
> are almost identical in their genetic makeup, as well?
Where do you get your ideas? The mice in question are all a single
species, with many partially isolated populations, whose boundaries
change over time. Mice and humans are not almost identical in their
genetic makeup. Mice differ from humans much more than chimpanzees do,
by any measure you care to name.
>>Fusion doesn't affect fertility very much, and in some
>>cases it doesn't affect it at all. How's that?
>
> too vague.
What else do you need?
>>>That said, the latest evidence in genome comparison between chimps and
>>>humans reveal an 83% difference between chimp chromosome 22 and human
>>>chromosome 21 (chimp chromosome 22 is said to be the ortholog of human
>>>chromosome 21.)
>>
>>I'm afraid you will have to tell us where you got that number, and what
>>it means. You have misunderstood something seriously, but I don't know
>>what. Ah, looking below I find you do tell us. The 83% difference is in
>>the location of recombination hot spots, not sequence. This would be a
>>very silly measure of genetic difference. In fact, as the press release
>>says, it doesn't seem to involve genetic differences at all. The DNA
>>sequence itself is still 99% identical.
>
>
> See:
>
> http://genomebiology.com/researchnews/default.asp?arx_id=gb-spotlight-20040528-01
I saw it. I have no idea what you think it means.
>>>And even though there appears to be 99% similarity
>>>between the DNA of humans and chimps, the recombination hot spots have
>>>turned out to be almost completely different. Apparently, then, DNA
>>>sequences, even though highly similar, do not determine biological
>>>function.
>>
>>Now that's a bundle of non sequiturs. Explain what you think you mean by
>>that. Of course they determine biological function. What they apparently
>>don't do is determine the sites at which recombination happens. That's
>>one biological function, not "biological function".
>
>
> bring this up again AFTER reading the above link.
I read it already. What do you think it means?
>>>It's like comparing the recipes for two cakes. They both use 99%
>>>similar ingredients -- flour, sugar, butter, eggs. Does this
>>>similarity mean that both cakes came from the same batter? Not
>>>necessarily. Not even probably. The more reasonable assumption is
>>>that both cakes were created in their own right, from different
>>>recipes, but using similar ingredients.
>>
>>This analogy has nothing at all to do with the similarity of DNA.
>>Further, the major evidence for common descent is not mere similarity,
>>but (have you heard this before?) nested hierarchy. Cakes just don't
>>display any such thing.
>
>
> every analogy breaks down sooner or later.
Yours break down sooner rather than later.
The former. Of course, you understand that you can karyotype individuals
and find out if they are hybrids between different chromosome numbers.
>>>>Or, take
>>>>the case of Przewalski's horse and the domestic horse: domestic horses, like
>>>>their human breeders, have one fewer chromosome pairs than their wild
>>>>ancestors, due, apparently, to a chromosomal fusion -- but domestic and
>>>>Przewalski's horses can still interbreed to produce fertile offspring. In
>>>>other cases (e.g. "chromosomal races" of mice), having different chromosome
>>>>numbers reduces interfertility.
>>>
>>>if you are comparing the horse scenario to the human/chimp scenario,
>>>you would need to explain why the domestic horse can still breed
>>>successfully with their wild ancestor, the Przewalski horse, and yet
>>>humans cannot breed with their supposed wild ancestor, the ape.
>>
>>Przewalski's horse is not the ancestor of domestic horses. It's a close
>>relative.
>
>
> well, Steven called it "ancestors." Could you and he come to some
> agreement?
Possibly.
>>The factors that allow or prevent interbreeding are complex,
>>but simple length of time apart is one of them.
>
>
> so would your theory predict that the Chinese race, living apart from
> the Indian race, would eventually, over time, evolve the inability to
> interbreed?
If that were true, then yes it would. However, no human population has
ever been that isolated. There is no Chinese race and no Indian race,
just clinal variation from one point to another.
Your diagram communicates nothing to me.
>>> Chimp ancestor population (24chrm)
>>>common ancestor (24 chrm) /_____________________
>>>___________________________/
>>> \
>>> \
>>> Human ancestor population (24chrm)
>>>
>>>At this point, there is as yet no change in the genetic makeup of
>>>either the chimp ancestor population or the human ancestor population.
>>>The only change is in geographical location which prevents Population
>>>A (containing a potential chimp ancestor) from interbreeding with
>>>Population B (containing a potential human ancestor).
>>>
>>>Right so far?
>>>
>>>Okay, so focusing now on the human ancestor population:
>>>
>>>Human ancestor population (24chrm)
>>>______________________________ /??
>>>
>>>What happens at this point? A fusion occurs in a single individual in
>>>this population, supposedly, right? I take it that the proposed rare
>>>beneficial mutations do not hit several members of the population at
>>>the same time? Otherwise they wouldn't be rare.
>>
>>Right. But nobody says this fusion is beneficial, and nobody says it's
>>the first difference to become fixed in the human lineage.
>
> so now evolutionary theory proposes that life forms evolve, not only
> from selected beneficial mutations, but from harmful and/or neutral
> mutations?
Yes. Does that come as a surprise? Harmful mutations are of course
eliminated, unless they're so slightly harmful as to be effectively neutral.
>>>Okay, so we now have a population of 24chrm members and one member's
>>>chromosomes 2a and 2b fuse into a single chromosome, forming
>>>chromosome 2 of the human ancestor's set of chromosomes.
>>>
>>>Supposedly, this 23chrm member of the 24chrm population can continue
>>>to interbreed with the 24chrm members, producing offspring that may or
>>>may not carry this 23chrm set. How does selection work in this case?
>>>Has it been demonstrated that Chromosome 2 in humans makes them
>>>distinctly different from apes, and gives them a distinct selective
>>>advantage?
>>
>>No. There's no reason to suppose it does.
>
>
> so how does your mechanism of selected beneficial mutation work then?
> If chromosome2 is the main piece of evidence that chimps and humans
> come from a common ancestor, and yet this piece of evidence makes no
> difference in the life form containing the fusion, what is there to
> select?
Chromosome 2 is by no means the main piece of evidence. And nobody says
that the fusion was selected.
>>>If not, it would be predicted that 23chrm members of the
>>>population would not necessarily increase but instead, as, they
>>>continue to interbreed, the 24chrm members will dominate because they
>>>are more in abundance, and the supposedly advantageous and distinct
>>>Chromosome 2 will die out and be lost to the population.
>>
>>You need to read up on genetic drift. Chromosomal mutations happen with
>>a certain frequency. Most are lost. By chance, a few increase in
>>frequency and eventually become fixed. This could easily be such a case.
>
> saying so doesn't make it so. Where's Deadrat when I need him. Maybe
> he could draw up a mathematical formula that will demonstrate how
> chance "beneficial" mutations that make no difference can get selected
> for.
I'm telling you they don't get selected for, and they're not beneficial.
Drift, not selection. Neutral, not beneficial.
> snip>
>
>>>>It doesn't seem likely that a modern human could (or at least would)
>>>>interbreed with a modern chimp, but presumably five million years ago, our
>>>>ancestors were just a tiny bit more "human" than the ancestors of modern
>>>>chimps.
>>>
>>>
>>>how can a life form be a tiny bit more human before it becomes human?
>>
>>How can it not? I don't understand your objection here. We're talking
>>about intermediates. Do you deny even the logical possibility of
>>intermediate forms?
>
> intermediate forms between an apple and a carrot? No. Intermediate
> forms between a carrot and a snail? No. Intermediate forms between
> a dinosaur and a bird? No.
Well, of course the first two are silly. The third sort are found in
fair profusion in the fossil record, e.g. Archaeopteryx. But were were
talking about human ancestry, yes?
>>>>They probably could have produced fertile offspring with the chimp
>>>>ancestors, but as noted, they lived in different parts of Africa and no
>>>>longer met.
>>>
>>>
>>>I note the use of "probably" here.
>>
>>Yes. That's because we don't know, and have no way of ever knowing,
>>exactly when reproductive isolatio evolved between the two lineages.
>
>
> I'm not asking for when it happened, but how it happened. So far, no
> steps have been given other than probabilities and maybes.
That's because we will never, ever know the details. We see the results
of 6 million years of evolution in two lineages, and you're asking to
see the order in which all the many changes occurred. How would that
even be possible?
Steven J.
> On Sun, 24 Jul 2005 00:59:10 -0500, "Steven J."
> <sjt195...@nts.link.net.INVALID> wrote:
>
bit confusing, but if we keep arguing this point without snipping out
anything, we're going to end up with posts the length of _Moby Dick_.
>
-- [snip]
>
>>No, parsimony rather than simple majority rule determines which (probably)
>>came first. "Parsimony," in this case, means accounting for the observed
>>pattern with the fewest postulated entities -- in this case, mutations.
>>If
>>the last common ancestor (LCA) of African apes had 23 chromosome pairs,
>>then
>>we need two mutations -- one to give the gorillas 24 pairs, and one to
>>give
>>the chimps 24 pairs -- to account for the observed distribution. If we
>>assume that the African ape LCA had 24 pairs, but the human-chimp LCA had
>>23
>>pairs, then we still need two mutations: one to reduce the number of pairs
>>after the human-chimp line splits from gorillas, and one to increase the
>>number of pairs in chimps after the human and chimp lines split. If we
>>assume that both the African ape and human-chimp LCA had 24 pairs, then we
>>need only one mutation to explain the difference (after the human-chimp
>>split). Of course, in some cases, parsimony will be *wrong* (nature
>>isn't,
>>as far as anyone knows, trying to keep mutations to a minimum), but it
>>seems
>>a good approximation most of the time.
>
> I see. I suppose that's a good speculative answer but not
> sufficiently scientific to hang an evolutionary cap upon. Call it a
> neutral position -- makes no difference one way or the other.
>
same assumptions -- used in reconstructing "phylogenies" of, e.g. multiple
variant copies of the _Canterbury Tales_, or the gospels, or chain letters.
I would think you would appreciate explanations that prefer the fewest
number of assumptions about unobserved events.
>
-- [snip]
>
>>When you say "83% difference," I'm not sure what you mean. If you mean
>>that
>>83% of the genes have at least one nucleotide different between the two
>>species, that is perfectly consistent with a 99% sequence similarity
>>between
>>the two chromosomes.
>
> see:
>
> http://genomebiology.com/researchnews/default.asp?arx_id=gb-spotlight-20040528-01
>
> Begin quote:
>
> 'Sakaki said their analysis found about 68,000 insertions or
> deletions. "That is almost one insertion/deletion every 470 bases," he
> said. In addition, a small proportion of genes showed a relatively
> higher rate of evolution than most other genes. "We haven't known what
> proportion of the genes shows adaptive evolution. This study shows it
> to be about 2 to 3%," he said.
>
amounts to a bit over one-fifth of one percent difference. If there are no
other differences in the genes besides those mentioned, then sequence
similarity between genes (as opposed to noncoding sequences) would be
something like 99.75%. Note that the authors distinguish between "adaptive
evolution" ("beneficial mutations") and, presumably, evolution that isn't
adaptive. If I'm reading this right, about 83% of the genes show *some*
difference (perhaps only one or two nucleotides altered), and about 3% of
genes show differences that resulted from beneficial mutations spreading
through natural selection, and the rest show differences that are inferred
to have arisen through neutral mutations that drifted to fixation. Of
course, this summary does not enable me to determine how they decided which
changes were adaptive and which were not.
>
> 'Early molecular comparisons between humans and chimpanzees suggested
> that the species are very similar to each other at the nucleotide
> sequence level - a difference of between 1.23% and 5%, Sakaki said.
> The results reported this week showed that "83% of the genes have
> changed between the human and the chimpanzee - only 17% are identical
> - so that means that the impression that comes from the 1.2%
> [sequence] difference is [misleading]. In the case of protein
> structures, it has a big effect," Sakaki said.'
>
previous estimates had made it, much less that the evidence for human-chimp
common ancestry is weaker than had previously been thought. Rather, the
point is that 1% sequence difference doesn't mean that only 1% of genes are
different (in principle, one could make a 1% difference in 100% of the
genes, or that the differences produce only a 1% difference in phenotype.
There's an analogy offered by some creationist sites: the sentences "All
competent biologists accept common descent" and "Not all competent
biologists accept common descent" have very high sequence similarity, but
opposite meanings. But the analogy works better for evolutionists:
obviously, one of those sentences is a modified copy of the other, and they
show how minor modifications can at once reveal common ancestry and produce
large changes.
>
> End quote.
>
> I recognize that this is written from an evolutionary point of view,
> so expect to find attempts to explain the differences in terms of
> change and loss or gain. But, really now, if a difference between the
> two is observed, there is nothing to say that the present difference
> is a result of change over millions of years, or if the difference was
> present from the time of origin.
>
true (although that vestigial centromere and telomere on chromosome 2 is
still very suggestive). But the strongest evidence for common descent is
not similarities between any two species, but the *nested hierarchy* of
similarities and differences for the huge number of known species.
If we had only two variant copies of some ancient manuscript, perhaps both
came from the hand of the original author, who revised his own first draft
slightly. But when we have dozens of copies, which naturally fall into
groups (sharing many similar readings), falling into larger groups (united
by a smaller number of readings shared by all the manuscripts in the larger
group) and so on, the idea that the original author didn't produce all these
copies, but that they were introduced gradually by different copyists at
different times, would become irresistable (especially if we already knew
about copyists and their errors).
Likewise, we know about mutations in living populations, and about the
nested hierarchies of related populations into which living species fall.
The overall pattern of life is simply a larger-scale version of the pattern
we see in populations *known* to be produced by common descent with
modification, whether cattle or silkworms or humans (or, for that matter,
families of languages and manuscripts).
>
> Further in the article, Derek Wildman tries to hold onto the idea that
> similarity must still mean relationship through a common ancestor, but
> I'm betting that with further comparison between the chimp genome and
> the human genome, this idea of relationship through a common ancestor
> will continue to degrade.
>
It has not "degraded" yet, so if it "degrades" in the future this will not
be a continuation of current trends. Noting that a lot of genes differ
between humans and chimps does not mean that the differences are at all
difficult to explain in terms of mutation and selection or drift, or even
that the number is greater than the theory of evolution (as opposed to
mathematically naive intuition) would lead us to expect.
>
>> Suppose (these figures are illustrative only; do not
>>assume they reflect actual measurements of the chromosome) that two
>>chromosomes in different species have 100 genes each. Suppose each gene
>>has
>>300 nucleotides, and that for each gene two nucleotides differ between the
>>two species. That would mean that on this chromosome, 100% of the genes
>>are
>>(slightly) different from their homologues in the other species, but that
>>overall sequence similarity is over 99%.
>
> Quoting further from the above link:
>
> 'Early molecular comparisons between humans and chimpanzees suggested
> that the species are very similar to each other at the nucleotide
> sequence level - a difference of between 1.23% and 5%, Sakaki said.
> The results reported this week showed that "83% of the genes have
> changed between the human and the chimpanzee - only 17% are identical
> - so that means that the impression that comes from the 1.2%
> [sequence] difference is [misleading]. In the case of protein
> structures, it has a big effect," Sakaki said.'
>
> End quote.
>
Zoe, the quoted passage and my own paragraph above do not contradict each
other in any respect. As noted above, "there is a 1.2% sequence difference"
is not the same thing as "1.2% of *genes* are different" -- 1.2% sequence
difference could mean that every single gene is, on average, 1.2% different
(which might produce no effects, or very profound effects, or about anything
in between), or it could mean that 1.6% of genes are 75% different from each
other, or some figure in between.
>
>> But certainly minor differences in
>>DNA sequence can produce major changes in function, and certainly genes by
>>themselves do not determine everything that happens in an organism.
>
> what are some other things, besides changes in genes, that are
> suggested would cause the kind of changes in an organism that would
> lead its population in a direction away from its old genus to a new
> one?
>
My point was that DNA, by itself, does nothing; only when combined with the
effects of the environment (which, for a gene, includes other genes, along
with ribosomes and other cellular systems) do genes produce any effects at
all. Changes outside the genes, if they could be inherited in some way
(e.g. taught by parents rather than passed on through sex cells), could
affect the way genes build an organism, or the selective pressures on genes,
or both. For example, if some ape *learns* to use a new food source (that
is, its genes are no different from those of other members of its species
who don't eat that food), and teaches its children to do likewise, this
could free the apes from some selective pressures (they wouldn't need to
compete so hard for older food sources), and create new selective pressures
(e.g. modifications in the digestive tract or other anatomical features to
enable them to better use the new food source).
>
-- [snip]
>
>>Actually, a sufficient similarity in composition (exact proportions of
>>many
>>minor ingredients) may strongly indicate origin from the same batter. At
>>least, this line of reasoning is commonly used in forensic science for
>>bullet fragments and dirt samples.
>
> we do not have access to exact proportions in biology. In forensic
> science, there is access to the original firearm and the original
> source of dirt for comparison purposes. Not so in biology.
>
We only know that it is the "original" firearm, or the "original" source of
dirt, based on the same sort of argument that you reject for genomes.
>
>> But in any case, a closer analogy to DNA
>>would be the exact wording of the recipes themselves -- especially if both
>>recipes shared the same mispellings of the same words in the same order,
>>and
>>had bits of text that were alike but didn't seem to have anything to do
>>with
>>the actual recipe (like, e.g. the pseudogenes and endogenous retroviruses
>>chimps and humans share).
>
> recipes aren't available biologically so the analogy falls apart at
> this point.
>
In the analogy, genes (or rather genomes) *are* the recipes. Certainly
genomes are available biologically.
>
> But, again, similarity is not sufficient to indicate relationship
> through a common ancestor, as is being seen in in the latest
> chimp/human genome comparisons.
>
I don't think you understand the latest human/chimp genome comparisons.
And, again, the argument for common descent is not based simply on
human/chimp similarities, but on the consistent ways in which we are more
similar to chimps than either of us is to gorillas, and so forth throughout
the nested hierarchy of life.
>
>>By the way, why is it more reasonable, even if we don't know for sure, to
>>suppose that the cakes were created from different recipes and different
>>batter?
>
> because, from experience, we know that cakes come from different
> batters. There is not one single grand clearing house of cake batter
> from which all cakes come.
>
Okay, you don't buy junk food. Good for you.
But we *do* know that living things come from other living things, that
reproduction is not quite perfect, and that mutations, natural selection,
and drift cause populations to evolve over time. We *do* know that
consistent nested hierarchies of inheritable traits result from branching
descent with modification, whether we're talking about breeds of domestic
animals, or viruses, or languages, and hand-copied biblical texts. There is
ample reason to infer that the nested hierarchy of life reflects a series of
more or less remote common ancestors.
>
>> Certainly a baker is capable of making one big batch of batter and
>>making lots of cakes from it.
>
> yes, but there is no single common source of batter to all cakes.
>
To paraphrase your own argument above, cake batter isn't available
biologically, so your analogy falls apart at this point.
>
>> And a Creator, I would suppose, is perfectly
>>capable of making many species from a single ancestral population, as He
>>made (according to the Bible) many nations from one original human
>>population.
>
> but we don't think that cakes and cars come from the same batter or
> assembly line, do we? There is no one common source of material to
> all categories of things, just as there is no one common ancestor to
> all categories of life forms.
>
Zoe, if you follow that analogy far enough, it implies that there is no
common Creator to all categories of life forms. If you don't follow it that
far, why should you expect me to follow it to imply that there is no common
ancestor to all known taxa?
>
-- [snip]
>
>>Okapis have no known subspecies; the variant chromosome numbers do not
>>correspond to racial or habitat differences. And, apparently, they
>>interbreed freely with okapis with different numbers of chromosomes and
>>produce fertile offspring. Google turns up a few scholarly articles on
>>"chromosomal polymorphism" in okapis and other species, and this appears,
>>in
>>okapis and some other species, to work like any other polymorphism (that
>>is,
>>it no more affects interbreeding than the difference between, say, type A
>>and type O blood, or blue and brown eyes).
>
> so these scholarly articles to which you refer, do they mention having
> tested the chromosomes of known parents to known offspring and having
> discovered that the chromosome counts differ in the parents? Or is
> the testing randomly done, without checking to see if those opaki with
> same chromosome counts might tend to be attracted to each other, or
> whether different chromosome-count opakis tend to repel each other?
>
I don't think they mention checking actual parentage for any okapis. I
doubt very much that okapis can tell how many chromosome pairs another
okapi has, but the presence of several okapis with odd numbers of
chromosomes strongly implies mating between okapis with different numbers of
chromosomes, at least in the past.
>
-- [snip]
>
>>There's no evidence that chimps with chromosomes 2a and 2b can interbreed
>>with gorillas with chromosomes 2a and 2b. They've spent seven million
>>years
>>or more evolving in different directions (not just in obvious anatomical
>>ways, but in more subtle ones). For all either of us knows, hominins (the
>>human side of the human-chimp lineage) and panins (the chimp side) stopped
>>being interfertile before the chromosome fusion happened in the hominin
>>line. I doubt that chromosome number per se is much of a guide to
>>interfertility.
>
> so it's just guesswork here at this point?
>
On some points, yes, it's pretty much guesswork. Are you hoping to argue
that if scientists don't know everything, they can't know anything, or that
all aspects of hominid phylogeny must be equally speculative (rather than
some parts virtually certain and others, as you note, mere guesswork)? Is
there any area of historical reconstruction of which this is true? It seems
to me that it is quite common to have the broad outlines of historical
events firmly established and amply supported by evidence, while the fine
details are sketchy and often poorly evidenced. It is the same with human
evolution.
>
>>But again, horse subspecies with different numbers of chromosomes are
>>interfertile. Okapis with a rather recent mutation that produced a fused
>>chromosome are interfertile. I'm speculating that what is known to happen
>>in several species today could have happened in other species at other
>>times; it seems a safe enough speculation.
>
> okay, it's still speculation. Moving on...
>
By "a safe enough speculation" I meant that we know, from experience, that
differing chromosome numbers, by themselves, do not lower interfertility
(although different chromosome numbers, plus other genetic and chromosomal
changes, will do this), so there is no reason at all to suppose that the
first hominid with 23 chromosome pairs would have any problems mating with
hominids of the same species, but with 24 pairs.
>
-- [snip of longish section that you did not challenge]
>
>>Right, except that population A contains many potential (indeed, *actual*)
>>chimp ancestors, as population B contains many human ancestors.
>
> so are you saying that many members of Population B got hit by the
> same rare benefit mutation, or are you saying that many members of
> Population B result from a single member getting hit by the rare
> beneficial mutation and passing it down to offspring?
>
Zoe, suppose a mutant ape (call him "Harvey") is born, long ago in Africa.
Suppose one of Harvey's two copies of chromosome 2a fused with a copy of
chromosome 2b, to produce fused chromosome 2. Harvey has 47 chromosomes
(since it inherited 23 chromosomes, including the fused chromosome, only
from one parent, and the "normal" 24 chromosomes from the other). This
mutation may be beneficial in some way, or purely neutral. Harvey grows up
and sires many ape babies, some of whom inherit its fused chromosome (others
inherit the unfused version, so some of its kids have 48 chromosomes and
some have 47). This goes on for many generations, until a generation comes
along in which two descedants of Harvey (both of whom have, unlike some of
Harvey's descendants, inherited this fused chromosome) mate and produce an
offspring with *two* copies of the fused chromosome. This sort of thing
goes on for many, many, many generations.
If the fused chromosomes are actually beneficial (maybe Harvey and some of
his descendants are smarter than the average ape), then apes with one copy
of the fused chromosome will mate more often and have more surviving
children (especially if the children have inherited the chromosome), and the
fused chromosome will spread through the population rapidly (in geological
time). If it is merely a neutral change, then it will be unlikely to spread
through the population -- but "unlikely" does not mean it will never happen,
and in some cases neutral mutations, over hundreds of generations, do spread
through the entire population. If the fused chromosomes produce a
deleterious effect -- if Harvey is dumber or clumsier than the average
ape -- the the fused chromosome will most likely go extinct in a few
generations (maybe just one, if Harvey dies without surviving offspring).
But then, since the fused chromosome did survive, presumably it wasn't
detrimental.
It works much the same for any mutation. There's no need for it to occur in
many members of the population at once (although it may -- some mutations
recur over and over). Note that even though, in the scenario above, every
member of the descendant population inherits Harvey's mutation, they aren't
the descendants of Harvey alone. They are, at least, the descendants of the
non-mutant (or at least, not carrying *this* particular mutation) female(s)
who bore Harvey's offspring. They are descendants of the males and females
who mated with Harvey's kids and grandkids. They are, in short, descended
from many of Harvey's contemporaries, and inherit, probably, many genes from
those contemporaries, even if not one copy of the unfused chromosomes 2a and
2b from those contemporaries has been passed on (if you have children, you
probably have alleles they didn't inherit -- since each child inherits only
a random half of your genes -- but they're still 100% your descendants).
>
> And I take it that Population A must have been hit with some other
> kind of rare beneficial mutation in order for it to begin to exhibit
> characteristics of chimpness?
>
There is no need for this to happen when it first branched off from
population B, but yes, in time, presumably mutants with favorable mutations
were born in population A on many occasions, over millions of years. Note,
by the way, that humans exhibit many characteristics of "chimpness" (Jared
Diamond wrote a book about our species called _The Third Chimpanzee_ --
bonobos are the second chimpanzee), and the human/chimp LCA presumably was
more chimplike than we are already.
>
>> Some
>>individuals in either population will end up having no living descendants,
>>but others will be the ancestor (if they're in population A) of every
>>chimpanzee alive today), or (if they're in population B) of every human
>>who's ever lived (and every Neanderthal, _Homo erectus_, australopith, and
>>so on). There is no one single mutant individual who is the sole ancestor
>>and cause of modern humans.
>
> well, it has got to start with a single member, unless you are
> proposing that the same rare beneficial mutation hits many members of
> the population at the same time or within a certain time frame?
>
No single mutation made us human, or a different species from the parents of
the mutant. We are descended from many, many individuals, most of them
"mutants" in the sense that some portion of some gene they have is slightly
different from any gene of either of their parents.
>
-- [snip]
>
>>There's no reason to suppose the change was beneficial, rather than
>>neutral.
>
> it has to be beneficial, according to your theory, in order to get
> selected. If it's neutral, there's nothing to select.
>
True. But in a sexually reproducing population, since only half the genes
get passed on to any offspring, if an organism has ten offspring, any given
gene has roughly 1 chance in 1024 of not being passed on at all. Likewise
any given gene has the same chance of being passed on to all ten offspring.
That sounds like tiny odds -- but apes have ca. 25,000 genes. Now, over
time and in a large population, favorable mutations will tend to spread
despite this, but some neutral variations will die out, and others will
spread to fixation, just by "chance," or, as it is technically known,
genetic drift.
>
>>There's been speculation that the change in chromosomal numbers was linked
>>to the emergence of some distinctively human trait (e.g. bipedalism), but
>>there's no evidence for that that I'm aware of. Again, note that
>>differences in chromosome numbers seem to make no difference to okapis;
>>it's
>>simply another way individuals in a population can vary.
>>
>>Now, if you have a neutral mutation (one that makes an individual neither
>>more nor less fit in that particular environment), then its survival in
>>each
>>generation is a matter of pure chance. Most neutral mutations presumably
>>die out in short order, swamped by the more common (even if no better)
>>alleles at that locus. But mathematical models show that, from time to
>>time, by sheer dumb luck, a neutral mutation will become more and more
>>common in each successive generation, until it completely replaces the
>>original trait.
>
> so the entire evolutionary framework consists of sheer dumb luck. Not
> very scientific or predictable, is it?
>
No, neutral drift consists of sheer dumb luck, which is a very different
matter from natural selection. Evolutionary theory encompasses both,
although evolutionists argue among themselves as to which explains more
genetic change over time (hardly anyone disputes that natural selection
explains *adaptive* change, but not all change is adaptive). Note that
sheer dumb luck is quite predictable, which is why Las Vegas casinos manage
to stay in business, and quite scientific, which is why probability and
statistics exist as branches of mathematics.
>
>>http://www.talkorigins.org/faqs/genetic-drift.html
>>
>>Humans and chimps have identical amino-acid sequences for the enzyme
>>cytochrome-c, but the *genes* for cytochrome-c differ in one nucleotide
>>between the two species (this is possible because there are multiple
>>three-nucleotide codons for each amino acid). This is a "silent" mutation
>>(one with no phenotypic effect), and surely neutral. It presumably
>>originated as a mutation in one individual in one species, and just by
>>sheer
>>dumb luck spread through that species over hundreds of generations. This
>>can also happen to traits that do make a difference, if the difference
>>doesn't affect chances of reproductive success. Perhaps the spread of the
>>fused chromosome was just a case of neutral drift.
>
> "presumably" "perhaps" "speculated" "sheer dumb luck" "seem to"
> "there's no evidence" "pure chance" -- sorry, Steven, but none of this
> sounds very scientific. And these terms are used in connection with
> the central core of your theory. How is this expected to command
> respect from any thinking but undecided person? Gravity, which many
> like to have placed in the same category as evolutionary theory, does
> not consist of a series of maybes and perhapses.
>
[a] Evolutionary theory does not consist of series of "perhapses and
maybes." On the other hand, reconstructions of specific evolutionary events
and series of events are like reconstructions of other historical phenomena.
Many histories of ancient empires and wars are full of such terms -- we have
the lists of kings and victories, the rough outlines of borders, the temples
and hymns to major gods, and the like, but the fine details of life,
religion, and politics are half guesswork. It is much the same with human
evolution; there is massive and firm evidence for the broad outlines of
phylogeny (and the *fact* of that phylogeny), but the details are, indeed,
rather speculative.
[b] No one knows what gravity *is*. There are detailed equations
describing how it works, but as to *why* it works that way, or whether
"gravitons" exist (theory predicts them, but they've never been detected),
and the like, are indeed "a series of maybes and perhapses." There's a lot
of math behind those maybes -- but then, there's more math than you seem to
grasp behind arguments over the relationships of extinct hominids.
[c] It seems to me that one can better command the respect of thinking and
undecided persons by frankly admitting when one did not know, or when the
evidence could be interpreted in many ways, or when the evidence was
absent -- this ought, I would think, increase the weight given to claims
that were not hedged about with such qualifications, because they *were*
strongly supported by evidence. I was going to make a snide comment about
thinking and undecided creationists here, but decided not to.
>
-- [snip]
>
>>As noted, this happens most of the time, with most neutral mutations, but
>>every so often you get an exception. Flip enough coins enough times, and
>>sooner or later one will come up "heads" over and over and over.
>
> your whole theory is built upon the flip of the coin. Still not a
> scientific approach.
>
Entire faculties of mathematical geneticists and molecular phylogenists will
be *so* sorry to hear (from someone who once argued that dividing by zero
gave meaningful results) that their fields of study are invalid and
unscientific.
>
-- [snsip]
>
>>Maybe nothing. Not all evolution is the result of natural selection.
>
> but natural selection is a biggie, isn't it? What's left?
>
Natural selection is a "biggie" when it comes to explaining adaptive changes
(changes that make organisms better able to find food, avoid becoming food,
and generally leave descendants). Not all changes are adaptive. Besides
natural selection there are, at least, sexual selection and genetic drift.
>
>> And
>>there are problems with describing selection pressures on populations
>>millioins of years ago.
>
> of course there are. So why the strident, dogmatic stance of so many
> posters on TO -- excluding you, of course.
>
Note that there are differences between "common descent" and mechanisms of
common descent. It is not unheard of to be able to say with immense and
justified confidence that something happened, and have only vague and
poorly-supported notions of *why* it happened. Think of the comments about
gravity above. Heck, think about the programming decisions of the major
television networks. For that matter, there is a difference between arguing
that natural selection *can* produce some effect, and showing that, in fact,
particular selective pressures *did* in fact produce that effect. I don't
think many of the posters who argue with you are strident and dogmatic about
the selective pressures at work in the past (although they may, perhaps, be
dogmatic about what selective pressures were *not* present -- see some
discussions of the "aquatic ape hypothesis").
>
>> There's a lot that isn't known about how genes
>>interact with each other and the environment to build an organism, and
>>it's
>>hard to say what the effect would be. Even if we could say what the
>>effect
>>would be, there's still the problem of figuring out why it would be
>>advantageous (there are several competing theories of why bipedalism, or
>>larger brains, or thinning body hair, would benefit our ancestors).
>
> thank you for a fair and impartial answer.
>
You're quite welcome.
>
-- [snip of matters dealt with, as best I can, above]
>
>>Of course I can argue that. As noted above, some neutral changes are
>>"silent," with no phenotypic effect.
>
> and selection works with phenotypic effect, I take it?
>
Yes, almost by definition.
>
>> But a change can produce a quite
>>marked effect, and still be "neutral" (that is, can make reproductive
>>success in the given environment neither more nor less likely).
>
> I didn't think that is what was meant by neutral mutations. There are
> two definitions that I see so far, used by evolutionists:
>
> 1) A mutation that has no effect on the Darwinian fitness of its
> carriers.
> 2) A mutation that has no phenotypic effect.
>
> Where is the "marked effect" in the above understanding of neutral
> mutations?
>
Any change that's obvious to an observer, but doesn't affect the organism's
odds of reproductive success.
>
>> There are
>>two vireo (a type of bird) species that humans can easily tell apart only
>>by
>>eye color. There's no reason to suppose that one eye color is better than
>>the other for the birds, but the difference distinguishes the two species.
>
> wait a minute. Does difference in eye color alone make a new species?
> Then a blue-eyed human is a different species from a brown-eyed human?
>
Difference in eye color is not the *only* difference between the two
species, I'm pretty sure, and I doubt it's the *cause* of speciation, but
it's the obvious difference. My point is that one species has one eye
color, and another species has another eye color, and there's no reason to
suppose that one eye color is an adaption to some aspect of the environment,
but it's an obvious (a "marked") difference. It's a visible analog to the
difference in chromosome numbers between humans and chimps. I could have
cited different color patterns seen in many "vicar" species (you remember
vicar species, I assume) to make the same point -- not all evolution is
adaption.
Note, although it's irrelevant to the exact point at hand, that differences
that cause speciation in one group of organisms might be irrelevant in
another. There are cichlid species that are kept separate, in the wild,
purely because they are different in color -- if you put them in an aquarium
under light that makes their colors indistinguishable, they will mate to
produce fertile offspring. It's quite conceivable that eye color alone
could make populations in *some* genus into separate species, even though it
obviously doesn't do that in humans.
>
>>Of course, the change might be beneficial in one population, because of
>>sexual selection (female fashion-consciousness), but that's not quite the
>>same thing as getting food more easily, avoiding becoming food, or
>>fighting
>>off infections better. Quite possibly some of the differences between
>>humans and chimps were sexually rather than "naturally" selected.
>
> add "quite possibly" to the dictionary of evolutionary theory. So far
> nothing scientific. What is scientific is the actual data. The
> theory proposed in regard to the data, however, being based on maybes
> and possiblies, is not scientific.
>
This has been dealt with above.
>
>>As argued above, the change in chromosome number was quite possibly a
>>"neutral" change, although it is clearly one of the differences between us
>>and chimps. Note that something like 90% of the genome is neither genes
>>nor
>>regulatory sequences.
>
> it would be expected that more than 90% of a cell's chromosomes (the
> genome) would have its genes turned off and unrecognizable as genes
> since only 3% or so of each cell's chromosomes have genes turned on to
> code for the protein making of that particular cell type. This does
> not mean that the noncoding material is junk. It just is not used for
> that particular cell's purpose. And I would expect that when not
> actively in use, the potential for gene formation sits around looking
> for all the world like junk.
>
You are confused, here. That 90% of the genome wasn't "turned on" in any
cell, ever. Actually, a rather higher percentage than that is never turned
on; to get to 10% you have to include DNA that is never transcribed into
proteins, but that seems to regulate which DNA is transcribed into proteins.
>
>> A lot of the 100 million or so differences between
>>the human and chimp genomes almost certainly don't make any difference
>>that
>>matters to us -- they are "information" if you're looking for differences
>>between human and chimp genomes, but if you're looking for "what makes us
>>human," they aren't "information" in whatever sense it is that
>>creationists
>>have in mind when they speak of "new information."
>
> I'm not following you here.
>
Most of the genetic differences between humans and chimps don't have any
effect on how we or chimps develop or behave. They are "silent" or
"neutral" mutations, and most of them are changes to DNA with no discernable
"function" except taking up space in the genome.
>
-- [snip]
>
>>Again, mathematical models suggest that very small differences in
>>"fitness"
>>can give a trait a big advantage over time.
>
> "small differences" aren't the same as neutral differences, are they?
>
No, and natural selection isn't the same as genetic drift.
>
>> So, for that matter, do actual
>>observations of microevolution in the wild: Grant's finches on the
>>Galapagos
>>had small differences in beak size and shape that hardly made them
>>different
>>species, or even different subspecies -- but made a real difference in
>>fitness.
>>>
>>>>It doesn't seem likely that a modern human could (or at least would)
>>>>interbreed with a modern chimp, but presumably five million years ago,
>>>>our
>>>>ancestors were just a tiny bit more "human" than the ancestors of modern
>>>>chimps.
>>>
>>> how can a life form be a tiny bit more human before it becomes human?
>
I'm going to address this again. _Ardipithecus ramidus_, whose spine
entered its skull at an angle in between the chimp and human angles, seems
to have been "a tiny bit more human" than the human-chimp LCA (assuming the
LCA had a fully-chimplike posture and gait). _Australopithecus_, with many
chimplike features but an erect gait and a brain that was large for a chimp
its size was "a tiny bit more human" than _Ardipithecus_. _Homo
rudolfensis_ was "a tiny bit more human" than the australopiths. _Homo
ergaster_ was "a tiny bit more human" than _H. rudolfensis_. If you don't
understand this, what about evolutionary theory can you hope to understand?
>
-- [snip of matters I tried to deal with above]
>
-- Steven J.
Steven J.
>
>>No, that's not a principle, but we can't discard his first reason. It's
>>not just numbers of species but the shape of the phylogenetic tree that
>>determines what came first.
>
> the shape of the phylogenetic tree is a subjective one, based on the
> subjective opinions of the taxonomist and cladist, right?
>
not subjective; it is the tree that best fits the evidence. John Harshman
wrote a "post of the month" that explains the reasoning behind this and the
math that supports the given tree over all other possible trees. The
"subjective decisions" are things like whether to class humans, chimps, and
gorillas all in the genus _Homo_, or as separate genera in the subfamily
Homininae. How you label the various splits is a different matter from
deciding in which order, or approximately when, they occurred. Labelling
is subjective (within limits); the splits and their order is objective.
>
>> Since we know the tree (i.e. that chimps,
>>gorillas, orangutans, and gibbons are successively less closely related
>>to humans),
>
> isn't this what is called assuming your conclusion? You say,
> authoritatively, We know that these creatures are successively less
> closely related to humans. How do we know this? By our phylogenetic
> tree that we have subjectively made up.
>
from and strongly supported by the data. See Harshman's
http://www.talkorigins.org/origins/postmonth/apr05.html for more details.
The phylogenic tree isn't offered as evidence, but as a graphic
representation of what is deduced from the pattern of similarities and
differences in different species.
>
>> we know what came first. Either 24 pairs came first (and
>>humans evolved 23), or chimps, gorillas, orangutans, and gibbons all
>>evolved 24 pairs independently from an ancestor with 23 pairs. Which
>>makes more sense to you?
>
> if I were forced to embrace evolutionary theory, I would have to say
> that fusion makes more sense than fission. But fission is just as
> plausible within the evolutionary framework in which many life forms
> emerge from a single common ancestor.
>
branch of the primate family tree) is more plausible than some combination
of of four fissions or fusions, all happening to the same chromosome, all in
the same closely-related group of species, while (despite how common
chromosome number changes would have to be in apes for this explanation to
be right) no other chromosomes in any ape species seem to have fused or
split.
>
-- [snip]
>
> if chromosome fusion is used as evidence of a split from a common
> ancestor population, does chromosome fusion in mice also represent a
> split from a common ancestor population, especially as mice and humans
> are almost identical in their genetic makeup, as well?
>
were descended from a common ancestral population of _Mus musculus_ -- that
is, that all house mice share, at some point, a common ancestor that was a
house mouse (even if that common ancestor didn't, at the time, live in
houses).
Zoe, you don't seem to be actually thinking about the evidence being
presented to you, or you just don't understand it. Chromosome fusion (or
fission, whichever) in mice isn't being offered as evidence that mice and
humans shared a common ancestor (*that* conclusion depends on the overall
fit of mice into the rodent nested hierarchy, and the fit of the rodent and
primate nested hierarchies into the overall mammal nested hierarchy,
including fossil species). It isn't being used, by itself, as evidence that
mice share common ancestors with anything (except other mice); it's being
used as evidence that differences in chromosome numbers can mean the
difference between different species, or different races in the same
species, or merely between different individuals in the same breeding
population.
>
>>Fusion doesn't affect fertility very much, and in some
>>cases it doesn't affect it at all. How's that?
>
> too vague.
>
How is it vague?
>
-- [snip]
>
>>Przewalski's horse is not the ancestor of domestic horses. It's a close
>>relative.
>
> well, Steven called it "ancestors." Could you and he come to some
> agreement?
>
John is the actual biologist and expert in molecular phylogenics. Assume
where we disagree on a question in biology (if, in fact, we actually are in
disagreement) that I am wrong and he is right.
>
>>The factors that allow or prevent interbreeding are complex,
>>but simple length of time apart is one of them.
>
> so would your theory predict that the Chinese race, living apart from
> the Indian race, would eventually, over time, evolve the inability to
> interbreed?
>
They don't live "apart" -- commerce and communication between the two
countries is ancient and continuing. How do you suppose that Buddhism -- a
religion that started in India -- became so common in China and other east
Asian lands? Gene flow between the two lands is not heavy, but neither is
it negligible, and different populations aren't likely to speciate as long
as they're exchanging genes with each other (although there's always
sympatric speciation to consider, I suppose).
>
-- [snip]
>
>>Right. But nobody says this fusion is beneficial, and nobody says it's
>>the first difference to become fixed in the human lineage.
>
> so now evolutionary theory proposes that life forms evolve, not only
> from selected beneficial mutations, but from harmful and/or neutral
> mutations?
>
Neutral drift (and "nearly-neutral drift") is thought to explain a lot of
nonadaptive evolution, yes.
>
-- [snip]
>
>>> how can a life form be a tiny bit more human before it becomes human?
>>
>>How can it not? I don't understand your objection here. We're talking
>>about intermediates. Do you deny even the logical possibility of
>>intermediate forms?
>
> intermediate forms between an apple and a carrot? No. Intermediate
> forms between a carrot and a snail? No. Intermediate forms between
> a dinosaur and a bird? No.
>
Carrots did not evolve into snails, or vice-versa; their last common
ancestor was a single-celled organism. Intermediate forms between nonavian
theropod dinosaurs and birds are embarrassingly abundant if you want to deny
that they are even logically possible: think _Archaeopteryx_,
_Sinosauropteryx_, _Microraptor_, _Confuciusornis_, etc. Why do you think
these cannot even conceivably be intermediate forms?
>
>>>> They probably could have produced fertile offspring with the chimp
>>>>ancestors, but as noted, they lived in different parts of Africa and no
>>>>longer met.
>>>
>>>
>>> I note the use of "probably" here.
>>
>>Yes. That's because we don't know, and have no way of ever knowing,
>>exactly when reproductive isolatio evolved between the two lineages.
>
> I'm not asking for when it happened, but how it happened. So far, no
> steps have been given other than probabilities and maybes.
>
You seem, at many places, to deny that it even *did* happen, so evidence
that it did happen is relevant and important, even if we can't provide you
with conclusive evidence as to how and why it happened.
>
-- Steven J.
Zoe
<sjt195...@nts.link.net.INVALID> wrote:
snip>
>Note that molecular phylogeny uses the same techniques -- and many of the
>same assumptions -- used in reconstructing "phylogenies" of, e.g. multiple
>variant copies of the _Canterbury Tales_, or the gospels, or chain letters.
>I would think you would appreciate explanations that prefer the fewest
>number of assumptions about unobserved events.
the problem is not with the number of assumptions. It is with the
fact that parsimony is applied to a situation in which numbers are
irrelevant. Random mutations have no order governing them. They can
happen often or little or not at all, according to sheer dumb luck, as
you put it. So to try to apply a principle of order and "how it
should be" to random activity would be useless, I think.
>-- [snip]
>>
>>>When you say "83% difference," I'm not sure what you mean. If you mean
>>>that
>>>83% of the genes have at least one nucleotide different between the two
>>>species, that is perfectly consistent with a 99% sequence similarity
>>>between
>>>the two chromosomes.
>>
>> see:
>>
>> http://genomebiology.com/researchnews/default.asp?arx_id=gb-spotlight-20040528-01
>>
>> Begin quote:
>>
>> 'Sakaki said their analysis found about 68,000 insertions or
>> deletions. "That is almost one insertion/deletion every 470 bases," he
>> said. In addition, a small proportion of genes showed a relatively
>> higher rate of evolution than most other genes. "We haven't known what
>> proportion of the genes shows adaptive evolution. This study shows it
>> to be about 2 to 3%," he said.
>>
>Now, if my math can be trusted, one insertion/deletion every 470 bases
>amounts to a bit over one-fifth of one percent difference. If there are no
>other differences in the genes besides those mentioned, then sequence
>similarity between genes (as opposed to noncoding sequences) would be
>something like 99.75%.
if sequence similarity between genes were truly 99.75%, then
morphologically, we would be 99.75% similar to chimps. Reality is, we
are not 99.75% similar to chimps in our outward appearance. Outward
appearance is a result of those same genes that are considered to be
almost identical to chimps.
> Note that the authors distinguish between "adaptive
>evolution" ("beneficial mutations") and, presumably, evolution that isn't
>adaptive. If I'm reading this right, about 83% of the genes show *some*
>difference (perhaps only one or two nucleotides altered), and about 3% of
>genes show differences that resulted from beneficial mutations spreading
>through natural selection, and the rest show differences that are inferred
>to have arisen through neutral mutations that drifted to fixation. Of
>course, this summary does not enable me to determine how they decided which
>changes were adaptive and which were not.
is there even a way to determine if a change is adaptive versus a
result of some rare "beneficial" mutation?
>> 'Early molecular comparisons between humans and chimpanzees suggested
>> that the species are very similar to each other at the nucleotide
>> sequence level - a difference of between 1.23% and 5%, Sakaki said.
>> The results reported this week showed that "83% of the genes have
>> changed between the human and the chimpanzee - only 17% are identical
>> - so that means that the impression that comes from the 1.2%
>> [sequence] difference is [misleading]. In the case of protein
>> structures, it has a big effect," Sakaki said.'
>>
>Again, the point is not that the sequence similarity is smaller than
>previous estimates had made it, much less that the evidence for human-chimp
>common ancestry is weaker than had previously been thought. Rather, the
>point is that 1% sequence difference doesn't mean that only 1% of genes are
>different (in principle, one could make a 1% difference in 100% of the
>genes, or that the differences produce only a 1% difference in phenotype.
>There's an analogy offered by some creationist sites: the sentences "All
>competent biologists accept common descent" and "Not all competent
>biologists accept common descent" have very high sequence similarity, but
>opposite meanings. But the analogy works better for evolutionists:
>obviously, one of those sentences is a modified copy of the other, and they
>show how minor modifications can at once reveal common ancestry and produce
>large changes.
in what way does the fact that you have two sentences, one starting
with "Not all...." and the other starting with "All..." mean common
ancestry in your analogy? And why does one sentence necessarily have
to be a modified copy of the other? The one sentence quite obviously
comes from a completely different source than the other. One from
creationists, the other from evolutionists.
>> End quote.
>>
>> I recognize that this is written from an evolutionary point of view,
>> so expect to find attempts to explain the differences in terms of
>> change and loss or gain. But, really now, if a difference between the
>> two is observed, there is nothing to say that the present difference
>> is a result of change over millions of years, or if the difference was
>> present from the time of origin.
>>
>If all we had to study were humans and chimps, that would be more or less
>true (although that vestigial centromere and telomere on chromosome 2 is
>still very suggestive). But the strongest evidence for common descent is
>not similarities between any two species, but the *nested hierarchy* of
>similarities and differences for the huge number of known species.
a nested hierarchy would only be strong evidence if there are no other
nested hierarchies that form in the real world. To ignore the fact
that there are other nested hierarchies in the real world that are not
a result of common descent, and then claim that this one particular
nested hierarchy must be the result of common descent, is to impose an
undue burden upon the one evolutionary hierarchy.
For the evolutionary understanding of nested hierarchy, see:
http://www.lobue.com/enterprise_evolution/knowledge_hierarchy.html
by the above evolutionary admission, there are other nested
hierarchies besides the biological hierarchies.
Nested hierarchy is just another term for levels of organization. You
find levels of organization in many other fields besides biology.
None of these other fields draw the conclusion that, therefore, common
source or ancestry is indicated.
Take, for instance, the following hierarchy for all humans.
Using geographical boundaries. North America: USA: Florida: Seminole
County: Orlando: 100 East Street: Human: John Doe.
Using ecological boundaries. Biome: Community: Population: Human:
John Doe.
Lo, we have a twin-nested hierarchy.
Here's another twin-nested hierarchy.
Population: John Doe: organ systems: organs: tissues: cells:
chromosomes: DNA.
and
Population: John Doe: brain, nervous system: neuron: dendrites/axons:
synapse: neurotransmitters.
So, does the ability to recognize hierarchies and/or twin-nested
hierarchies mean anything more than we are able to classify things
hierarchically?
>If we had only two variant copies of some ancient manuscript, perhaps both
>came from the hand of the original author, who revised his own first draft
>slightly. But when we have dozens of copies, which naturally fall into
>groups (sharing many similar readings), falling into larger groups (united
>by a smaller number of readings shared by all the manuscripts in the larger
>group) and so on, the idea that the original author didn't produce all these
>copies, but that they were introduced gradually by different copyists at
>different times, would become irresistable (especially if we already knew
>about copyists and their errors).
are you proposing here that the first common ancestor was as complex
as an intelligently produced manuscript? Or has your analogy broken
down before it even started?
>Likewise, we know about mutations in living populations, and about the
>nested hierarchies of related populations into which living species fall.
>The overall pattern of life is simply a larger-scale version of the pattern
>we see in populations *known* to be produced by common descent with
>modification, whether cattle or silkworms or humans (or, for that matter,
>families of languages and manuscripts).
the principle of common descent does not hold when applied to all
other twin-nested hierarchies. Why should it hold just for biological
life forms?
>> Further in the article, Derek Wildman tries to hold onto the idea that
>> similarity must still mean relationship through a common ancestor, but
>> I'm betting that with further comparison between the chimp genome and
>> the human genome, this idea of relationship through a common ancestor
>> will continue to degrade.
>>
>It has not "degraded" yet, so if it "degrades" in the future this will not
>be a continuation of current trends. Noting that a lot of genes differ
>between humans and chimps does not mean that the differences are at all
>difficult to explain in terms of mutation and selection or drift, or even
>that the number is greater than the theory of evolution (as opposed to
>mathematically naive intuition) would lead us to expect.
well, the term used in the article was "misleading."
"... the impression that comes from the 1.2% [sequence] difference is
[misleading]."
What impression is this that is misleading, if not the impression that
we are so nearly identical to chimps that we must have come from a
common ancestor?
rather than speculate as to what the 1.2% difference means, it might
help to just take what Sakaki says at face value. He says that the
current impression is misleading.
>>> But certainly minor differences in
>>>DNA sequence can produce major changes in function, and certainly genes by
>>>themselves do not determine everything that happens in an organism.
>>
>> what are some other things, besides changes in genes, that are
>> suggested would cause the kind of changes in an organism that would
>> lead its population in a direction away from its old genus to a new
>> one?
>>
>My point was that DNA, by itself, does nothing; only when combined with the
>effects of the environment (which, for a gene, includes other genes, along
>with ribosomes and other cellular systems) do genes produce any effects at
>all. Changes outside the genes, if they could be inherited in some way
>(e.g. taught by parents rather than passed on through sex cells), could
>affect the way genes build an organism, or the selective pressures on genes,
>or both. For example, if some ape *learns* to use a new food source (that
>is, its genes are no different from those of other members of its species
>who don't eat that food), and teaches its children to do likewise, this
>could free the apes from some selective pressures (they wouldn't need to
>compete so hard for older food sources), and create new selective pressures
>(e.g. modifications in the digestive tract or other anatomical features to
>enable them to better use the new food source).
isn't that Lamarck? Wikipedia says that Lamarckism holds that traits
acquired (or diminished) during the lifetime of an organism can be
passed on to the offspring.
>-- [snip]
>>
>>>Actually, a sufficient similarity in composition (exact proportions of
>>>many
>>>minor ingredients) may strongly indicate origin from the same batter. At
>>>least, this line of reasoning is commonly used in forensic science for
>>>bullet fragments and dirt samples.
>>
>> we do not have access to exact proportions in biology. In forensic
>> science, there is access to the original firearm and the original
>> source of dirt for comparison purposes. Not so in biology.
>>
>We only know that it is the "original" firearm, or the "original" source of
>dirt, based on the same sort of argument that you reject for genomes.
I meant that we have access to the original firearm or dirt. We do
not have access to the original ancestors for comparison purposes.
>>> But in any case, a closer analogy to DNA
>>>would be the exact wording of the recipes themselves -- especially if both
>>>recipes shared the same mispellings of the same words in the same order,
>>>and
>>>had bits of text that were alike but didn't seem to have anything to do
>>>with
>>>the actual recipe (like, e.g. the pseudogenes and endogenous retroviruses
>>>chimps and humans share).
>>
>> recipes aren't available biologically so the analogy falls apart at
>> this point.
>>
>In the analogy, genes (or rather genomes) *are* the recipes. Certainly
>genomes are available biologically.
the genomes of the early ancestors are not available. We are
comparing the present DNA makeup with what is supposed to have been in
the common ancestor, aren't we?
>> But, again, similarity is not sufficient to indicate relationship
>> through a common ancestor, as is being seen in in the latest
>> chimp/human genome comparisons.
>>
>I don't think you understand the latest human/chimp genome comparisons.
>And, again, the argument for common descent is not based simply on
>human/chimp similarities, but on the consistent ways in which we are more
>similar to chimps than either of us is to gorillas, and so forth throughout
>the nested hierarchy of life.
not only is similarity not a good basis on which to conclude
relationship, but the classification itself is entirely subjective.
>>>By the way, why is it more reasonable, even if we don't know for sure, to
>>>suppose that the cakes were created from different recipes and different
>>>batter?
>>
>> because, from experience, we know that cakes come from different
>> batters. There is not one single grand clearing house of cake batter
>> from which all cakes come.
>>
>Okay, you don't buy junk food. Good for you.
I'm curious as to how you drew that conclusion.
>But we *do* know that living things come from other living things, that
>reproduction is not quite perfect, and that mutations, natural selection,
>and drift cause populations to evolve over time. We *do* know that
>consistent nested hierarchies of inheritable traits result from branching
>descent with modification, whether we're talking about breeds of domestic
>animals, or viruses, or languages, and hand-copied biblical texts. There is
>ample reason to infer that the nested hierarchy of life reflects a series of
>more or less remote common ancestors.
once again, the ability to classify objects based on similarity does
not necessarily mean common ancestry. If, as a rule, similarity
always meant relationship (not to mention common ancestry), then
evolutionists would have a point. "Looks like" is too superficial to
carry much weight.
>>> Certainly a baker is capable of making one big batch of batter and
>>>making lots of cakes from it.
>>
>> yes, but there is no single common source of batter to all cakes.
>>
>To paraphrase your own argument above, cake batter isn't available
>biologically, so your analogy falls apart at this point.
cake batter is an attempt to analogize your common ancestor. At that
point, it has not yet fallen apart. There is no single source of
batter to all cakes, just as there is no single common ancestor to all
life forms.
>>> And a Creator, I would suppose, is perfectly
>>>capable of making many species from a single ancestral population, as He
>>>made (according to the Bible) many nations from one original human
>>>population.
>>
>> but we don't think that cakes and cars come from the same batter or
>> assembly line, do we? There is no one common source of material to
>> all categories of things, just as there is no one common ancestor to
>> all categories of life forms.
>>
>Zoe, if you follow that analogy far enough, it implies that there is no
>common Creator to all categories of life forms.
there is a difference between the creator and the created. The
Creator is apart from the created. You can have a creator who is
common to all his creation. You don't have a creation that is common
to all other creation.
> If you don't follow it that
>far, why should you expect me to follow it to imply that there is no common
>ancestor to all known taxa?
because intelligence is known to create in a nested hierarchical
fashion. Created items are not known to organize themselves into such
patterns. It's as simple as that -- observation of how intelligence
(or mental activity) works, versus stupidity (or mindless activity).
In every area it works the same except when it comes to evolutionary
theory. Why is that? Is it a wish to not acknowledge a mind that
could be of superior intelligence to ours?
>-- [snip]
>>
>>>Okapis have no known subspecies; the variant chromosome numbers do not
>>>correspond to racial or habitat differences. And, apparently, they
>>>interbreed freely with okapis with different numbers of chromosomes and
>>>produce fertile offspring. Google turns up a few scholarly articles on
>>>"chromosomal polymorphism" in okapis and other species, and this appears,
>>>in
>>>okapis and some other species, to work like any other polymorphism (that
>>>is,
>>>it no more affects interbreeding than the difference between, say, type A
>>>and type O blood, or blue and brown eyes).
>>
>> so these scholarly articles to which you refer, do they mention having
>> tested the chromosomes of known parents to known offspring and having
>> discovered that the chromosome counts differ in the parents? Or is
>> the testing randomly done, without checking to see if those opaki with
>> same chromosome counts might tend to be attracted to each other, or
>> whether different chromosome-count opakis tend to repel each other?
>>
>I don't think they mention checking actual parentage for any okapis. I
>doubt very much that okapis can tell how many chromosome pairs another
>okapi has,
of course, they would not be expected to know the chromosome count of
each other -- leave that to be investigated by the researcher. But it
would be expected that the mere existence of differing chromosome
counts would produce differing kinds of proteins such that,
instinctively, the "same-counts" opakis would gravitate to each other.
> but the presence of several okapis with odd numbers of
>chromosomes strongly implies mating between okapis with different numbers of
>chromosomes, at least in the past.
has this been observed, is the question. Has it been investigated and
found that two parents of a particular offspring had different
chromosome counts?
>-- [snip]
>>
>>>There's no evidence that chimps with chromosomes 2a and 2b can interbreed
>>>with gorillas with chromosomes 2a and 2b. They've spent seven million
>>>years
>>>or more evolving in different directions (not just in obvious anatomical
>>>ways, but in more subtle ones). For all either of us knows, hominins (the
>>>human side of the human-chimp lineage) and panins (the chimp side) stopped
>>>being interfertile before the chromosome fusion happened in the hominin
>>>line. I doubt that chromosome number per se is much of a guide to
>>>interfertility.
>>
>> so it's just guesswork here at this point?
>>
>On some points, yes, it's pretty much guesswork. Are you hoping to argue
>that if scientists don't know everything, they can't know anything, or that
>all aspects of hominid phylogeny must be equally speculative (rather than
>some parts virtually certain and others, as you note, mere guesswork)?
no, but guesswork must be recognized as guesswork and not fact.
> Is
>there any area of historical reconstruction of which this is true? It seems
>to me that it is quite common to have the broad outlines of historical
>events firmly established and amply supported by evidence, while the fine
>details are sketchy and often poorly evidenced. It is the same with human
>evolution.
that's just it. What you consider to be broad outlines firmly
established, I have yet to see those broad outlines established by
anything more than maybe or probably.
>>>But again, horse subspecies with different numbers of chromosomes are
>>>interfertile. Okapis with a rather recent mutation that produced a fused
>>>chromosome are interfertile. I'm speculating that what is known to happen
>>>in several species today could have happened in other species at other
>>>times; it seems a safe enough speculation.
>>
>> okay, it's still speculation. Moving on...
>>
>By "a safe enough speculation" I meant that we know, from experience, that
>differing chromosome numbers, by themselves, do not lower interfertility
and that was my question. For those species that have differing
chromosome numbers, have they tested the parents to see if they indeed
had differeing chromosome numbers, or did they just test random
members of populations and conclude that therefore,
different-chromosome members were able to interbreeded and produce
fertile offspring?
>(although different chromosome numbers, plus other genetic and chromosomal
>changes, will do this), so there is no reason at all to suppose that the
>first hominid with 23 chromosome pairs would have any problems mating with
>hominids of the same species, but with 24 pairs.
until the above question is answered, there is every reason to
question whether some fantasized first hominid with 23 chromosomes was
able to interbreed with one with 24 pairs.
you do realize that the entire scenario you painted above is a
speculative one, containing no hard facts?
>It works much the same for any mutation.
and from the above speculative scenario it is concluded,
authoritatively, that, therefore, it woks much the same for any
mutation?
> There's no need for it to occur in
>many members of the population at once (although it may -- some mutations
>recur over and over). Note that even though, in the scenario above, every
>member of the descendant population inherits Harvey's mutation, they aren't
>the descendants of Harvey alone. They are, at least, the descendants of the
>non-mutant (or at least, not carrying *this* particular mutation) female(s)
>who bore Harvey's offspring. They are descendants of the males and females
>who mated with Harvey's kids and grandkids. They are, in short, descended
>from many of Harvey's contemporaries, and inherit, probably, many genes from
>those contemporaries, even if not one copy of the unfused chromosomes 2a and
>2b from those contemporaries has been passed on (if you have children, you
>probably have alleles they didn't inherit -- since each child inherits only
>a random half of your genes -- but they're still 100% your descendants).
supposition is not science. Until you can demonstrate that Harvey and
his kids followed the scenario that you painted for them, it remains a
just-so story used to prop up evolutionary theory.
>> And I take it that Population A must have been hit with some other
>> kind of rare beneficial mutation in order for it to begin to exhibit
>> characteristics of chimpness?
>>
>There is no need for this to happen when it first branched off from
>population B, but yes, in time, presumably mutants with favorable mutations
>were born in population A on many occasions, over millions of years. Note,
>by the way, that humans exhibit many characteristics of "chimpness" (Jared
>Diamond wrote a book about our species called _The Third Chimpanzee_ --
>bonobos are the second chimpanzee), and the human/chimp LCA presumably was
>more chimplike than we are already.
similarities are made to carry far more weight than they can truly
carry. Steven, so far, all you're giving me are presumptions.
Presumptions are not science.
>>> Some
>>>individuals in either population will end up having no living descendants,
>>>but others will be the ancestor (if they're in population A) of every
>>>chimpanzee alive today), or (if they're in population B) of every human
>>>who's ever lived (and every Neanderthal, _Homo erectus_, australopith, and
>>>so on). There is no one single mutant individual who is the sole ancestor
>>>and cause of modern humans.
>>
>> well, it has got to start with a single member, unless you are
>> proposing that the same rare beneficial mutation hits many members of
>> the population at the same time or within a certain time frame?
>>
>No single mutation made us human, or a different species from the parents of
>the mutant. We are descended from many, many individuals, most of them
>"mutants" in the sense that some portion of some gene they have is slightly
>different from any gene of either of their parents.
I didn't say that a single mutation made an ape human. I said that
the first single mutation has to hit a single individual, unless you
think that the same rare mutation hits many members of the population
at the same time.
>-- [snip]
>>
>>>There's no reason to suppose the change was beneficial, rather than
>>>neutral.
>>
>> it has to be beneficial, according to your theory, in order to get
>> selected. If it's neutral, there's nothing to select.
>>
>True.
true. You said "true." That answer is sufficient, so leave it at
that. What follows does not address what I just said.
probability and statistics has nothing to do with organization and
building and creating. It just says what are the chances of something
happening. Once the thing happens, probability and statistics can
only say what are the chances that such a thing can happen again. You
don't use probability and statistics to build something in an orderly
and methodical manner.
Explain to me how you build a digestive system via the mechanism of
blind, sheer dumb luck. Or make it easier. Explain how you would
build a cardboard box via the mechanism of sheer dumb luck.
>>>http://www.talkorigins.org/faqs/genetic-drift.html
>>>
>>>Humans and chimps have identical amino-acid sequences for the enzyme
>>>cytochrome-c, but the *genes* for cytochrome-c differ in one nucleotide
>>>between the two species (this is possible because there are multiple
>>>three-nucleotide codons for each amino acid). This is a "silent" mutation
>>>(one with no phenotypic effect), and surely neutral. It presumably
>>>originated as a mutation in one individual in one species, and just by
>>>sheer
>>>dumb luck spread through that species over hundreds of generations. This
>>>can also happen to traits that do make a difference, if the difference
>>>doesn't affect chances of reproductive success. Perhaps the spread of the
>>>fused chromosome was just a case of neutral drift.
>>
>> "presumably" "perhaps" "speculated" "sheer dumb luck" "seem to"
>> "there's no evidence" "pure chance" -- sorry, Steven, but none of this
>> sounds very scientific. And these terms are used in connection with
>> the central core of your theory. How is this expected to command
>> respect from any thinking but undecided person? Gravity, which many
>> like to have placed in the same category as evolutionary theory, does
>> not consist of a series of maybes and perhapses.
>>
>[a] Evolutionary theory does not consist of series of "perhapses and
>maybes."
well, those are the words used when describing it.
> On the other hand, reconstructions of specific evolutionary events
>and series of events are like reconstructions of other historical phenomena.
>Many histories of ancient empires and wars are full of such terms -- we have
>the lists of kings and victories, the rough outlines of borders, the temples
>and hymns to major gods, and the like, but the fine details of life,
>religion, and politics are half guesswork. It is much the same with human
>evolution; there is massive and firm evidence for the broad outlines of
>phylogeny (and the *fact* of that phylogeny), but the details are, indeed,
>rather speculative.
I'm afraid, from what you've described so far, the broad outlines are
also speculative.
>
>[b] No one knows what gravity *is*. There are detailed equations
>describing how it works, but as to *why* it works that way, or whether
>"gravitons" exist (theory predicts them, but they've never been detected),
>and the like, are indeed "a series of maybes and perhapses." There's a lot
>of math behind those maybes -- but then, there's more math than you seem to
>grasp behind arguments over the relationships of extinct hominids.
gravity is not in the same class as evolutionary theory. Making the
comparison doesn't fool anyone who is thinking outside the
evolutionary box.
>
>[c] It seems to me that one can better command the respect of thinking and
>undecided persons by frankly admitting when one did not know, or when the
>evidence could be interpreted in many ways, or when the evidence was
>absent -- this ought, I would think, increase the weight given to claims
>that were not hedged about with such qualifications, because they *were*
>strongly supported by evidence. I was going to make a snide comment about
>thinking and undecided creationists here, but decided not to.
very noble of you.
>-- [snip]
>>
>>>As noted, this happens most of the time, with most neutral mutations, but
>>>every so often you get an exception. Flip enough coins enough times, and
>>>sooner or later one will come up "heads" over and over and over.
>>
>> your whole theory is built upon the flip of the coin. Still not a
>> scientific approach.
>>
>Entire faculties of mathematical geneticists and molecular phylogenists will
>be *so* sorry to hear (from someone who once argued that dividing by zero
>gave meaningful results) that their fields of study are invalid and
>unscientific.
making fun of my dividing by zero doesn't work here because I made it
clear that I was thinking outside of the mathematical box. It turned
out to be quite an interesting mental exercise for me.
As to the part played by a flip of a coint. It would be observed that
systems are not put together by the mechanism of flipping coins. We
were discussing how systems are put together, whether by intelligence
or random activity. Coin flipping is random, and no one would dare to
say that coin flipping works for building systems -- except
evolutionists, I guess.
>-- [snsip]
>>
>>>Maybe nothing. Not all evolution is the result of natural selection.
>>
>> but natural selection is a biggie, isn't it? What's left?
>>
>Natural selection is a "biggie" when it comes to explaining adaptive changes
>(changes that make organisms better able to find food, avoid becoming food,
>and generally leave descendants). Not all changes are adaptive. Besides
>natural selection there are, at least, sexual selection and genetic drift.
none of these carry the weight you would like them to carry. Sorry.
>>> And
>>>there are problems with describing selection pressures on populations
>>>millioins of years ago.
>>
>> of course there are. So why the strident, dogmatic stance of so many
>> posters on TO -- excluding you, of course.
>>
>Note that there are differences between "common descent" and mechanisms of
>common descent. It is not unheard of to be able to say with immense and
>justified confidence that something happened, and have only vague and
>poorly-supported notions of *why* it happened.
in real science, one does not say, with immense and justified
confidence, that something definitely happened a certain way, when all
that supports such an idea are speculative notions on HOW it happened.
> Think of the comments about
>gravity above. Heck, think about the programming decisions of the major
>television networks. For that matter, there is a difference between arguing
>that natural selection *can* produce some effect, and showing that, in fact,
>particular selective pressures *did* in fact produce that effect. I don't
>think many of the posters who argue with you are strident and dogmatic about
>the selective pressures at work in the past (although they may, perhaps, be
>dogmatic about what selective pressures were *not* present -- see some
>discussions of the "aquatic ape hypothesis").
I find that the aquatic ape theory is another example of fantasy gone
haywire. There are no facts to support it, as far as I can see.
snip>
>>>Of course I can argue that. As noted above, some neutral changes are
>>>"silent," with no phenotypic effect.
>>
>> and selection works with phenotypic effect, I take it?
>>
>Yes, almost by definition.
and that is why chromosome 2 is the death knell to the chimp/human
relationship. If chromosome 2 is 99% identical to chromosomes 2a and
b in apes, then humans, phenotypically, should be 99% similar to apes.
We are not. So then you would have to say that the 1% difference is
what has caused the differences. Phenotypically, apes (or chimps) and
humans are NOT 1% different.
>>> But a change can produce a quite
>>>marked effect, and still be "neutral" (that is, can make reproductive
>>>success in the given environment neither more nor less likely).
>>
>> I didn't think that is what was meant by neutral mutations. There are
>> two definitions that I see so far, used by evolutionists:
>>
>> 1) A mutation that has no effect on the Darwinian fitness of its
>> carriers.
>> 2) A mutation that has no phenotypic effect.
>>
>> Where is the "marked effect" in the above understanding of neutral
>> mutations?
>>
>Any change that's obvious to an observer, but doesn't affect the organism's
>odds of reproductive success.
chromosome2 is not obvious to an observer, is it? It shouldn't get
selected.
>>> There are
>>>two vireo (a type of bird) species that humans can easily tell apart only
>>>by
>>>eye color. There's no reason to suppose that one eye color is better than
>>>the other for the birds, but the difference distinguishes the two species.
>>
>> wait a minute. Does difference in eye color alone make a new species?
>> Then a blue-eyed human is a different species from a brown-eyed human?
>>
>Difference in eye color is not the *only* difference between the two
>species, I'm pretty sure, and I doubt it's the *cause* of speciation, but
>it's the obvious difference.
eye color is an obvious difference that means nothing to the point you
were trying to make, I don't think.
> My point is that one species has one eye
>color, and another species has another eye color, and there's no reason to
>suppose that one eye color is an adaption to some aspect of the environment,
>but it's an obvious (a "marked") difference.
who said that eye color is an adaptation? I gave two reasons for
variation. One is variation as a result of recombination, just for
the sake of variation. And one is variation as a result of
adaptation, for the sake of coping with environmental stimuli.
> It's a visible analog to the
>difference in chromosome numbers between humans and chimps. I could have
>cited different color patterns seen in many "vicar" species (you remember
>vicar species, I assume) to make the same point -- not all evolution is
>adaption.
not all variation is adaptation, I agree.
>Note, although it's irrelevant to the exact point at hand, that differences
>that cause speciation in one group of organisms might be irrelevant in
>another. There are cichlid species that are kept separate, in the wild,
>purely because they are different in color -- if you put them in an aquarium
>under light that makes their colors indistinguishable, they will mate to
>produce fertile offspring. It's quite conceivable that eye color alone
>could make populations in *some* genus into separate species, even though it
>obviously doesn't do that in humans.
more speculation. We need hard facts -- evidence.
>>>Of course, the change might be beneficial in one population, because of
>>>sexual selection (female fashion-consciousness), but that's not quite the
>>>same thing as getting food more easily, avoiding becoming food, or
>>>fighting
>>>off infections better. Quite possibly some of the differences between
>>>humans and chimps were sexually rather than "naturally" selected.
>>
>> add "quite possibly" to the dictionary of evolutionary theory. So far
>> nothing scientific. What is scientific is the actual data. The
>> theory proposed in regard to the data, however, being based on maybes
>> and possiblies, is not scientific.
>>
>This has been dealt with above.
sorry, I'm afraid not, Steven.
>>>As argued above, the change in chromosome number was quite possibly a
>>>"neutral" change, although it is clearly one of the differences between us
>>>and chimps. Note that something like 90% of the genome is neither genes
>>>nor
>>>regulatory sequences.
>>
>> it would be expected that more than 90% of a cell's chromosomes (the
>> genome) would have its genes turned off and unrecognizable as genes
>> since only 3% or so of each cell's chromosomes have genes turned on to
>> code for the protein making of that particular cell type. This does
>> not mean that the noncoding material is junk. It just is not used for
>> that particular cell's purpose. And I would expect that when not
>> actively in use, the potential for gene formation sits around looking
>> for all the world like junk.
>>
>You are confused, here. That 90% of the genome wasn't "turned on" in any
>cell, ever.
and how did you decide this? In another cell, a different set of
genes are turned on. How do you know that this new set didn't come
from the 90% that was turned off and unrecognizable in another cell?
> Actually, a rather higher percentage than that is never turned
>on; to get to 10% you have to include DNA that is never transcribed into
>proteins, but that seems to regulate which DNA is transcribed into proteins.
>>
>>> A lot of the 100 million or so differences between
>>>the human and chimp genomes almost certainly don't make any difference
>>>that
>>>matters to us -- they are "information" if you're looking for differences
>>>between human and chimp genomes, but if you're looking for "what makes us
>>>human," they aren't "information" in whatever sense it is that
>>>creationists
>>>have in mind when they speak of "new information."
>>
>> I'm not following you here.
>>
>Most of the genetic differences between humans and chimps don't have any
>effect on how we or chimps develop or behave. They are "silent" or
>"neutral" mutations, and most of them are changes to DNA with no discernable
>"function" except taking up space in the genome.
so you can't count these neutral mutations as evolutionary. There is
nothing new or advantageous to select from. And you can't count the
harmful mutations, that's for sure. So you're back to building your
theory on some fantasized rare "beneficial mutations."
It's a rickety structure that won't stand up to the evidence.
>-- [snip]
>>
>>>Again, mathematical models suggest that very small differences in
>>>"fitness"
>>>can give a trait a big advantage over time.
>>
>> "small differences" aren't the same as neutral differences, are they?
>>
>No,
the answer is no. Adding anything more just muddies the answer.
> and natural selection isn't the same as genetic drift.
>>
>>> So, for that matter, do actual
>>>observations of microevolution in the wild: Grant's finches on the
>>>Galapagos
>>>had small differences in beak size and shape that hardly made them
>>>different
>>>species, or even different subspecies -- but made a real difference in
>>>fitness.
>>>>
>>>>>It doesn't seem likely that a modern human could (or at least would)
>>>>>interbreed with a modern chimp, but presumably five million years ago,
>>>>>our
>>>>>ancestors were just a tiny bit more "human" than the ancestors of modern
>>>>>chimps.
>>>>
>>>> how can a life form be a tiny bit more human before it becomes human?
>>
>I'm going to address this again. _Ardipithecus ramidus_, whose spine
>entered its skull at an angle in between the chimp and human angles, seems
>to have been "a tiny bit more human" than the human-chimp LCA (assuming the
>LCA had a fully-chimplike posture and gait). _Australopithecus_, with many
>chimplike features but an erect gait and a brain that was large for a chimp
>its size was "a tiny bit more human" than _Ardipithecus_. _Homo
>rudolfensis_ was "a tiny bit more human" than the australopiths. _Homo
>ergaster_ was "a tiny bit more human" than _H. rudolfensis_. If you don't
>understand this, what about evolutionary theory can you hope to understand?
what I understand is that a lot of speculative ideas are put forward
as fact. They are the ungrounded assumptions upon which evolutionary
theory teeters and totters.
Zoe
<jharshman....@pacbell.net> wrote:
snip>
zoe asked:
>> have they checked the parents of particular offspring and found that
>> different-numbered genomes were able to interbreed? Or did they
>> simply test various members, found that some have a certain number
>> chromosome count, and others a different count, and assumed that
>> different counts could interbreed?
>
>The former. Of course, you understand that you can karyotype individuals
>and find out if they are hybrids between different chromosome numbers.
karyotyping an individual does not tell you that two different
chromosome-numbered parents interbred. It simply tells you that the
individual ended up with too many or too few chromosomes. How does
this happen?
see:
http://gslc.genetics.utah.edu/units/disorders/karyotype/karyotypeinfo.cfm
Quote:
"How can cells end up with too many or too few chromosomes?
"Sometimes chromosomes are incorrectly distributed into the egg or
sperm cells during meiosis. When this happens, one cell may get two
copies of a particular chromosome, while another cell gets none."
End quote.
a different count of chromosomes, as seen in karyotyping, does not
mean that two parents with different counts interbred, but simply that
the chromosomes got incorrectly distributed during meiosis.
snip>
>>>The factors that allow or prevent interbreeding are complex,
>>>but simple length of time apart is one of them.
>>
>>
>> so would your theory predict that the Chinese race, living apart from
>> the Indian race, would eventually, over time, evolve the inability to
>> interbreed?
>
>If that were true, then yes it would. However, no human population has
>ever been that isolated. There is no Chinese race and no Indian race,
>just clinal variation from one point to another.
my point was, according to evolutionary ideas, if there are groups of
Chinese that have never been to India, and groups of Indians that
never went to China, would members of those particular groups, should
they ever meet after thousands of years, be unable to interbreed?
snip the rest of John's non-answers>
Zoe
Okay, here's the core of John's argument:
--Quote:
"Here is a set of DNA sequences. They come from two mitochondrial
genes, ND4 and ND5. If you put them together, they total 694
nucleotides. But most of those nucleotides either are identical among
all the species here, or they differ in only one species. Those are
uninformative about relationships, so I have removed them, leaving 76
nucleotides that make some claim. I'll let you look at them for a
while.
[ 10 20 30 40 50]
[ . . . . .]
+ 1 2++ 3 11 +4 3 ++ 52+1 2615+4 14+ 3 3+6+
gibbon ACCGCCCCCA TCCCCTCCCT CAAGTCCTAT CCAATCTACT GTACTTTGCC
orangutan ACCACTCCCA CCCTTCCTCC TAAGACTCAC ACAACTCGCC ACACCTCGTC
human GTCATCATCC TTCTTTTTTT AGGAATTTCC TCTCTCCGTC ACGCTCTACT
chimpanzee ATTACCATTC CTTTTTTCCC CGGATTCTCC CTTCTTCATT ATGTCTCATT
gorilla GTTGTTATTA CCTCCCTTTC AAGAACCCCT TTCACCTATC GCGTCCCACT
[ 60 70 ]
[ . . ]
+++ +++1 + +? 2 + +++
gibbon CCTACAGCCC AGCCAAACGA CACTAA
orangutan CCTACCGCCT AGCCATTTCA CACTAA
human CCCCTTATTT TCTTGTCCGG TGACCG
chimpanzee TTCCTCATTT TCTTACTCAG TGACCG
gorilla TTCCTTATTC TTTCGCCTAG TGATTA
I've marked with a plus sign all those sites at which gibbon and
orangutan match each other, and the three African apes (including
humans) have a different base but match each other. These sites all
support a relationship among the African apes, exclusive of gibbon and
orangutan. You will note there are quite a lot of them, 24 to be
exact. The sites I have marked with numbers from 1-6 contradict this
relationship. (Sites without numbers don't have anything to say about
this particular question.) We expect a certain amount of this because
sometimes the same mutation will happen twice in different lineages;
we call that homoplasy. However you will note that there are fewer of
these sites, only 22 of them, and more importantly they contradict
each other. Each number stands for a different hypothesis of
relationships; for example, number one is for sites that support a
relationship betwen gibbons and gorillas, and number two is for sites
that support a relationship between orangutans and gorillas (all
exclusive of the rest). One and two can't be true at the same time. So
we have to consider each competing hypothesis separately. If you do
that it comes out this way:
hypothesis sites supporting
African apes (+) 24
gibbon+gorilla (1) 6
orangutan+gorilla (2) 4
gibbon+human (3) 4
gibbon+chimp (4) 3
orangutan+human (5) 2
orangutan+chimp (6) 2
I think we can see that the African ape hypothesis is way out front,
and the others can be attributed to random homoplasy. This result
would be very difficult to explain by chance."
--End quote.
Well, I'm not going to even consider the statistical test John applies
to his idea above, because already the above is based on a faulty
premise. You can have a faulty premise and everything works after
that, even unto the math and statistics, but the conclusion will still
be false, regardless of how well the math works, simply because the
premise itself was false.
What is John's premise in the above comparisons? That DNA sequences
that are alike mean relationship. He chooses 76 nucleotides that make
some "claim," as he puts it. The claim, I take it, is that these
sequences are unique to both humans and chimps. Armed with this
similarity, and the faulty premise that similarity must mean
relationship, he proceeds to show how much more similar the
human/chimp relationships are than any other primate.
Well, big whoopdeedoo.
I can decide that similarity between computer-generated characters
means that they are related, too. I can point out where the
similarities lie, and how much more similar certain computer-generated
characters are than others. That does not make the characters any
more related to each other, just by my setting up some unsupported
standard that says similarity means relationship.
First John needs to establish the validity of his premise, that
similarity HAS to mean relationship. He has not done so.
snip>
Steven J.
> On Mon, 25 Jul 2005 01:33:57 -0500, "Steven J."
> <sjt195...@nts.link.net.INVALID> wrote:
>
>
> the problem is not with the number of assumptions. It is with the
> fact that parsimony is applied to a situation in which numbers are
> irrelevant. Random mutations have no order governing them. They can
> happen often or little or not at all, according to sheer dumb luck, as
> you put it. So to try to apply a principle of order and "how it
> should be" to random activity would be useless, I think.
>
there be -- such a thing as a "mutation rate?" For that matter, how could
there be "hot spots" on chromosomes where mutations are more likely than at
other loci? "Random," with respect to mutations, does not mean that the
mutations occur for no reason, or that all mutations are equally likely, or
that there is no possibility of saying how likely a mutation is to occur.
It means simply that the causes of the mutations, and the causes that make
some traits beneficial and others harmful, are not related to one another.
For that matter, again, if random events had no order governing them, then
probability as a field of mathematics could not exist. Your position as
stated above is pure obstinant folly.
>
-- [snip]
>
> if sequence similarity between genes were truly 99.75%, then
> morphologically, we would be 99.75% similar to chimps. Reality is, we
> are not 99.75% similar to chimps in our outward appearance. Outward
> appearance is a result of those same genes that are considered to be
> almost identical to chimps.
>
There is no one-to-one mapping between genotype and phenotype. A tiny
alteration in a gene can have an immense effect on how the organism
develops, or, conversely, very large changes in multiple genes can have no
effect at all. It has been known for a long time (since well before the
discovery of genes) that tiny changes in developmental rates (e.g. how long
a particular structure continues to grow) can produce immense differences in
how an organism looks -- and tiny changes in development rates can result
from tiny changes in genes. OTOH, as noted, large sections of many proteins
(and hence the genes that code for them) can be replaced with completely
different sequences without affecting function. Consider how many genetic
disorders are the result of changing one amino acid in one protein (the
result of changing one nucleotide in one gene). Equally drastic effects
that are not disorders can be produced by equally small changes.
>
>> Note that the authors distinguish between "adaptive
>>evolution" ("beneficial mutations") and, presumably, evolution that isn't
>>adaptive. If I'm reading this right, about 83% of the genes show *some*
>>difference (perhaps only one or two nucleotides altered), and about 3% of
>>genes show differences that resulted from beneficial mutations spreading
>>through natural selection, and the rest show differences that are inferred
>>to have arisen through neutral mutations that drifted to fixation. Of
>>course, this summary does not enable me to determine how they decided
>>which
>>changes were adaptive and which were not.
>
> is there even a way to determine if a change is adaptive versus a
> result of some rare "beneficial" mutation?
>
"Beneficial" mutations are by definition "adaptive," since both "beneficial"
and "adaption" are diagnosed because they enhance the organism's chances of
surviving and reproducing in a particular environment. Not all adaptive
change is the result of mutations: it may be that the "fitter" or better
adapted alleles are already present in the population, and simply become
more common due to natural selection. "Adaptive" evolution simply means
that alleles that are more beneficial become more common, whether those
alleles arise from new mutations or have been present since the parent
population first evolved.
>
-- [snip]
>
>>Again, the point is not that the sequence similarity is smaller than
>>previous estimates had made it, much less that the evidence for
>>human-chimp
>>common ancestry is weaker than had previously been thought. Rather, the
>>point is that 1% sequence difference doesn't mean that only 1% of genes
>>are
>>different (in principle, one could make a 1% difference in 100% of the
>>genes, or that the differences produce only a 1% difference in phenotype.
>>There's an analogy offered by some creationist sites: the sentences "All
>>competent biologists accept common descent" and "Not all competent
>>biologists accept common descent" have very high sequence similarity, but
>>opposite meanings. But the analogy works better for evolutionists:
>>obviously, one of those sentences is a modified copy of the other, and
>>they
>>show how minor modifications can at once reveal common ancestry and
>>produce
>>large changes.
>
> in what way does the fact that you have two sentences, one starting
> with "Not all...." and the other starting with "All..." mean common
> ancestry in your analogy? And why does one sentence necessarily have
> to be a modified copy of the other? The one sentence quite obviously
> comes from a completely different source than the other. One from
> creationists, the other from evolutionists.
>
Actually, in the original example, both sentences came from a creationist;
when I retyped the sentences, both came from someone who accepted evolution.
But the point is that any reasonable person (must present company be
excluded?) would infer that one of those two sentences was the original, and
the other was derived by either adding or removing the initial "not."
>
-- [snip]
>
> a nested hierarchy would only be strong evidence if there are no other
> nested hierarchies that form in the real world. To ignore the fact
> that there are other nested hierarchies in the real world that are not
> a result of common descent, and then claim that this one particular
> nested hierarchy must be the result of common descent, is to impose an
> undue burden upon the one evolutionary hierarchy.
>
Strictly speaking, one can arrange any set of entities in a nested
hierarchy. Anyone who's ever written an outline for a paper, or tried to
sort books in a library, has arranged ideas or objects in a nested
hierarchy. Note, though, that for many sets of objects, there are multiple
equally valid hierarchical arrangements of the objects. A book on, e.g.
_The History of the Spread of the Great Plague_ might be filed under
"History," or "Epidemiology," or "Diseases." One can arrange automobiles in
many different nested hierarchies: arrange them by manufacturer (e.g. GM
cars, and within that category Dodges, Cadillacs, Chevrolets, etc.), or by
type of vehicle (e.g. sedans, and under sedans GM sedans, Ford sedans,
etc.), or by various other schemes. One can always get a nested hierarchy,
but the hierarchy one gets depends on the traits one selects to compare.
What makes biology interesting is that one can pick many different sets of
traits to compare, and get the *same* nested hierarchy. The most-cited
example is the hierarchy formed by comparison of anatomical features and
that formed by comparing genes and proteins (the "twin nested hierarchy),
but one can see the same thing just be comparing, say, anatomical features.
All organisms with one bone in the lower jaw and three in the middle ear
also have mammary glands, and none have feathers. There's no obvious
reason, assuming separate origins, for that feature -- why not bats with
feathers, or penguins with mammary glands? *Consistent* nested hierarchies
do not arise through known methods of design -- human engineers cross-copy
components into very different designs (e.g. CD players installed in both GM
sedans and Ford trucks). Nature does not: pterosaurs and bats, although
both used furry membranous wings, use different ways of modifying forelimbs
to produce those wings.
>
> For the evolutionary understanding of nested hierarchy, see:
>
> http://www.lobue.com/enterprise_evolution/knowledge_hierarchy.html
>
This is astonishing. You may just have found the worst explanation of what
evolutionists mean by "nested hierarchy" on the entire World Wide Web (this
is not to say that the explanation is useless for other purposes). I would
suggest, rather,
http://www.talkorigins.org/faqs/comdesc/CDhierarchy.html
http://www.talkorigins.org/faqs/comdesc/CDhierarchy.html
http://www.isss.org/hierarchy.htm
>
> by the above evolutionary admission, there are other nested
> hierarchies besides the biological hierarchies.
>
> Nested hierarchy is just another term for levels of organization. You
> find levels of organization in many other fields besides biology.
> None of these other fields draw the conclusion that, therefore, common
> source or ancestry is indicated.
>
Actually, a "nested" hierarchy has not merely levels of organization, but
the lower levels form parts of the higher levels, as, e.g. "primates" are
part of the "mammals," which are part of the "vertebrates."
>
> Take, for instance, the following hierarchy for all humans.
>
> Using geographical boundaries. North America: USA: Florida: Seminole
> County: Orlando: 100 East Street: Human: John Doe.
>
John Doe is not a geographical feature; he is not part of East Street, or
part of the geography of Seminole County. Note, furthermore, that [a] if
John Doe moves to California, he ceases to be part of Seminole County in any
sense, and [b] John Doe can, as you note below, be classified as part of a
quite different nested hierarchy. Again, you are ignoring the salient and
compelling nature of the consistent nested hierarchies in biology.
>
> Using ecological boundaries. Biome: Community: Population: Human:
> John Doe.
>
> Lo, we have a twin-nested hierarchy.
>
No, you have two quite different nested hierarchies containing the same
entity. Again, one can construct nested hierarchies for any set of objects
or ideas, but the distinctive feature of life is that it falls into pretty
much the same hierarchy no matter what traits one seeks to compare.
>
> Here's another twin-nested hierarchy.
>
> Population: John Doe: organ systems: organs: tissues: cells:
> chromosomes: DNA.
>
> and
>
> Population: John Doe: brain, nervous system: neuron: dendrites/axons:
> synapse: neurotransmitters.
>
> So, does the ability to recognize hierarchies and/or twin-nested
> hierarchies mean anything more than we are able to classify things
> hierarchically?
>
>>If we had only two variant copies of some ancient manuscript, perhaps both
>>came from the hand of the original author, who revised his own first draft
>>slightly. But when we have dozens of copies, which naturally fall into
>>groups (sharing many similar readings), falling into larger groups (united
>>by a smaller number of readings shared by all the manuscripts in the
>>larger
>>group) and so on, the idea that the original author didn't produce all
>>these
>>copies, but that they were introduced gradually by different copyists at
>>different times, would become irresistable (especially if we already knew
>>about copyists and their errors).
>
> are you proposing here that the first common ancestor was as complex
> as an intelligently produced manuscript? Or has your analogy broken
> down before it even started?
>
Extant manuscripts only let us reconstruct the *last* common ancestor, not
the first. Variant manuscripts of the gospels enable scholars to
reconstruct (with some uncertainty) the text from which they were all
derived, but they are less informative about the process by which the
gospels originated, or what earlier lost forms of the gospels might have
existed. The same problem exists with life: the last common ancestor need
not have been -- presumably was not -- the *first* common ancestor.
>
>>Likewise, we know about mutations in living populations, and about the
>>nested hierarchies of related populations into which living species fall.
>>The overall pattern of life is simply a larger-scale version of the
>>pattern
>>we see in populations *known* to be produced by common descent with
>>modification, whether cattle or silkworms or humans (or, for that matter,
>>families of languages and manuscripts).
>
> the principle of common descent does not hold when applied to all
> other twin-nested hierarchies. Why should it hold just for biological
> life forms?
>
As noted, sets of phenomena that fall into consistent nested hierarchies
(basically the same hierarchy is derived regardless of the set of traits
used for comparison) do not typically result except from common descent.
Designed things, like cars or airplanes, not only diverge into variant
designs, but as designers modify them they copy features from one line of
descent into some items from other lines of descent (e.g. one manufacturer
introduces windshield wipers, and soon others add them to their models).
Designers don't "reinvent the wheel," they just copy already existing wheel
designs. Life (e.g. different wing designs in birds, bats, and pterosaurs,
different thumb designs in primates and pandas, different box-camera eye
designs in cephalopods and vertebrates) reinvents the wheel all the time.
>
-- [snip]
>
> well, the term used in the article was "misleading."
>
> "... the impression that comes from the 1.2% [sequence] difference is
> [misleading]."
>
> What impression is this that is misleading, if not the impression that
> we are so nearly identical to chimps that we must have come from a
> common ancestor?
>
That surely cannot be the meaning intended by the author, who is clearly an
evolutionist. The "misleading impression" is that if only a tiny percentage
of the sequence is different, then only a tiny percentage of genes can be
different, or perhaps that if only a tiny percentage of the genotype
differs, the phenotypes likewise must be only slightly different.
>
-- [snip]
>
> rather than speculate as to what the 1.2% difference means, it might
> help to just take what Sakaki says at face value. He says that the
> current impression is misleading.
>
And he does *not* say that this casts any doubt on human-chimp common
ancestry, and indeed assumes such common ancestry in his analysis. You are
not taking his words at face value; you are trying to force-fit them into a
creationist framework.
>
-- [snip]
>
>>My point was that DNA, by itself, does nothing; only when combined with
>>the
>>effects of the environment (which, for a gene, includes other genes, along
>>with ribosomes and other cellular systems) do genes produce any effects at
>>all. Changes outside the genes, if they could be inherited in some way
>>(e.g. taught by parents rather than passed on through sex cells), could
>>affect the way genes build an organism, or the selective pressures on
>>genes,
>>or both. For example, if some ape *learns* to use a new food source (that
>>is, its genes are no different from those of other members of its species
>>who don't eat that food), and teaches its children to do likewise, this
>>could free the apes from some selective pressures (they wouldn't need to
>>compete so hard for older food sources), and create new selective
>>pressures
>>(e.g. modifications in the digestive tract or other anatomical features to
>>enable them to better use the new food source).
>
> isn't that Lamarck? Wikipedia says that Lamarckism holds that traits
> acquired (or diminished) during the lifetime of an organism can be
> passed on to the offspring.
>
Lamarckianism means one or more of the following:
[a] Changes to the phenotype (whether the result of injury, learning, or
whatnot) can alter the genotype; the contrary idea is called "Weismannism"
(oddly, this idea was held by both Lamarck and Darwin, and is not essential
to either theory, but the winners write the history books, and the
Darwinists and Weismannists won).
[b] There is an "evolutionary ladder" from "lower" to "higher" forms, and
different species (or "kinds") evolved from separately originating lineages
that climbed this ladder over time (so, e.g. monkeys do not share common
ancestry with humans, but have evolved the same way we did, but not so far
as we have). Evolution has the "goal" of reaching the top of the ladder,
and all lineages are climbing the same ladder, but are on different rungs.
[c] Populations are propelled up the evolutionary ladder by some innate
force that acts upon their "need" to evolve and become better. Another
force adapts them to local variants of the environment.
The idea that there might be nongenetic influences on development, and
nongenetic paths of inheritance, is not Lamarckian in any of these senses.
>
-- [snip]
>
>>In the analogy, genes (or rather genomes) *are* the recipes. Certainly
>>genomes are available biologically.
>
> the genomes of the early ancestors are not available. We are
> comparing the present DNA makeup with what is supposed to have been in
> the common ancestor, aren't we?
>
It seems to me that we are attempting to reconstruct (in some cases) the DNA
(or some of it) from common ancestors, based on comparisons of the DNA of
living species -- just as a Biblical textual critic attempts to reconstruct
the original wording of the Bible by comparing different surviving texts,
not (of course) the lost ancient manuscripts themselves.
>
-- [snip]
>
>>I don't think you understand the latest human/chimp genome comparisons.
>>And, again, the argument for common descent is not based simply on
>>human/chimp similarities, but on the consistent ways in which we are more
>>similar to chimps than either of us is to gorillas, and so forth
>>throughout
>>the nested hierarchy of life.
>
> not only is similarity not a good basis on which to conclude
> relationship, but the classification itself is entirely subjective.
>
You persistently confuse the subjective *labelling* branch points with the
methods used to determine the branch points themselves, which are not
subjective.
>
>>>>By the way, why is it more reasonable, even if we don't know for sure,
>>>>to
>>>>suppose that the cakes were created from different recipes and different
>>>>batter?
>>>
>>> because, from experience, we know that cakes come from different
>>> batters. There is not one single grand clearing house of cake batter
>>> from which all cakes come.
>>>
>>Okay, you don't buy junk food. Good for you.
>
> I'm curious as to how you drew that conclusion.
>
Because junk food is made from huge batches of batter from which thousands
and thousands of snack food items are made. All twinkies, in fact, come
from one single grand clearing house of twinkie ingredients. It was a joke,
Zoe.
>
-- [snip]
>
> because intelligence is known to create in a nested hierarchical
> fashion. Created items are not known to organize themselves into such
> patterns. It's as simple as that -- observation of how intelligence
> (or mental activity) works, versus stupidity (or mindless activity).
> In every area it works the same except when it comes to evolutionary
> theory. Why is that? Is it a wish to not acknowledge a mind that
> could be of superior intelligence to ours?
>
Well, in a sense, at least one created object -- language -- organizes
itself into nested hierarchies. Humans don't try to change their languages
into new languages (although they add new words and slang), so, e.g. the
change of Latin into Spanish, French, Italian, etc. is unplanned and more an
attribute of the way language works than of human design. Furthermore,
humans deliberately confuse, to some extent, the nested hierarchy into which
languages natural fall as they differentiate from one another, by borrowing
words, and even sounds and grammatical features from one language into
another. So we see in language how consistent nested hierarchies result
from undesigned change, while designed change produces violations of
consistent nested hierarchies. A similar argument applies, as noted, to
automobiles, televisions, and other artifacts of known designers.
>
-- [snip]
>
> of course, they would not be expected to know the chromosome count of
> each other -- leave that to be investigated by the researcher. But it
> would be expected that the mere existence of differing chromosome
> counts would produce differing kinds of proteins such that,
> instinctively, the "same-counts" opakis would gravitate to each other.
>
There's no reason to suppose the proteins would differ; the genes themselves
are not changed (at least not as the result of chromosome fusion or
fission); they are not even moved relative to the genes near them on the
chromosome. The effect is like combining two encyclopedia volumes into one,
or splitting one into two: it doesn't change the articles themselves.
>
>> but the presence of several okapis with odd numbers of
>>chromosomes strongly implies mating between okapis with different numbers
>>of
>>chromosomes, at least in the past.
>
> has this been observed, is the question. Has it been investigated and
> found that two parents of a particular offspring had different
> chromosome counts?
>
It has certainly been done with domestic horses and Pzewalski's horses; I do
not know if it has been done with okapis.
>
-- [snip]
>
>>(although different chromosome numbers, plus other genetic and chromosomal
>>changes, will do this), so there is no reason at all to suppose that the
>>first hominid with 23 chromosome pairs would have any problems mating with
>>hominids of the same species, but with 24 pairs.
>
> until the above question is answered, there is every reason to
> question whether some fantasized first hominid with 23 chromosomes was
> able to interbreed with one with 24 pairs.
>
As noted, it works with horses and mice of different chromosomal races, so
there is, in fact, no reason to question whether it would be possible with
the first hominin with 47 chromosomes (he would, I presume, have one copy
each of chromosomes 2a and 2b, and one copy of the fused chromosome 2).
>
-- [snip]
I was attempting to illustrate to you how a mutation occurring in a single
individual could become fixed (homozygous in 100% of the population) over
time. It was offered as an illustration, not as supporting data for a
theory.
>
>>It works much the same for any mutation.
>
> and from the above speculative scenario it is concluded,
> authoritatively, that, therefore, it woks much the same for any
> mutation?
>
No, from my knowledge of how mutations and inheritance work, I concluded
that it works much the same for any mutation. You have this bad habit (it
seems common in creationists, but that's no excuse) for mistaking
illustrations of conclusions (e.g. the above scenario, or the phylogenic
trees of primates, or a reconstruction of an "ape-man") with the evidence
from which the conclusions were drawn (and, of course, if the pictures or
stories were the evidence, then the conclusions would indeed be weakly
supported).
>
-- [snip]
>
>>No, neutral drift consists of sheer dumb luck, which is a very different
>>matter from natural selection. Evolutionary theory encompasses both,
>>although evolutionists argue among themselves as to which explains more
>>genetic change over time (hardly anyone disputes that natural selection
>>explains *adaptive* change, but not all change is adaptive). Note that
>>sheer dumb luck is quite predictable, which is why Las Vegas casinos
>>manage
>>to stay in business, and quite scientific, which is why probability and
>>statistics exist as branches of mathematics.
>
> probability and statistics has nothing to do with organization and
> building and creating. It just says what are the chances of something
> happening. Once the thing happens, probability and statistics can
> only say what are the chances that such a thing can happen again. You
> don't use probability and statistics to build something in an orderly
> and methodical manner.
>
Some orderly systems do, in fact, arise from purely stochastic processes,
but that is not my point.
>
> Explain to me how you build a digestive system via the mechanism of
> blind, sheer dumb luck. Or make it easier. Explain how you would
> build a cardboard box via the mechanism of sheer dumb luck.
>
I have distinguished between adaptive evolution (which I attribute to
natural selection of mutations), and nonadaptive evolution, which I have
attributed largely to genetic drift ("dumb luck"). Digestive systems are
adaptions. Please try harder to understand the arguments directed at you.
>
-- [snip of Zoe repeating "unfounded assumptions" and "guesses" a lot]
When you are prepared to think about the arguments presented to you, we can
continue.
>
-- Steven J.
Steven J.
> On Mon, 25 Jul 2005 02:11:31 -0500, "Steven J."
> <sjt195...@nts.link.net.INVALID> wrote:
>
>>
>>"Zoe" <muz...@aol.com> wrote in message
>>news:6vn8e1h4rfl6ag833...@4ax.com...
>
>
>>> isn't this what is called assuming your conclusion? You say,
>>> authoritatively, We know that these creatures are successively less
>>> closely related to humans. How do we know this? By our phylogenetic
>>> tree that we have subjectively made up.
>>>
>>No, the phylogenic tree is a conclusion which was not assumed, but
>>inferred
>>from and strongly supported by the data. See Harshman's
>>http://www.talkorigins.org/origins/postmonth/apr05.html for more details.
>>The phylogenic tree isn't offered as evidence, but as a graphic
>>representation of what is deduced from the pattern of similarities and
>>differences in different species.
>
> Okay, here's the core of John's argument:
>
>
> Well, I'm not going to even consider the statistical test John applies
> to his idea above, because already the above is based on a faulty
> premise. You can have a faulty premise and everything works after
> that, even unto the math and statistics, but the conclusion will still
> be false, regardless of how well the math works, simply because the
> premise itself was false.
>
First, you have asserted many times that the phylogenic tree is
"subjective." Now, perhaps I've misunderstood you, but I took that to mean
that you felt that, even assuming common ancestry, there was no objective,
testable basis for preferring the conclusion that humans and chimps were
more closely related to each other than to orangutans, than for preferring
the conclusion that humans and orangutans were most closely related.
Clearly, there *is* an objective, testable basis for preferring some
phylogenic trees over others. Even if the premise of common descent is
false, the phylogeny is not purely subjective.
Second, don't you find it rather odd, if the premise of common descent is
false, that multiple lines of evidence converge on the same phylogeny?
Harshman picked a particular set of genes to compare, but one could reach
the same conclusion by examining other genes, or noncoding DNA sequences, or
proteins. If all the hominoid (ape + human) species are separately created,
why do they fall into the sort of pattern we would expect if they were
produced by braching descent from a common ancestor? If apes, or some apes,
are derived by descent with modification from an ape common ancestor, but
humans are separately created, why do comparisons consistently put humans
closer to African apes than to Asian apes -- and closer to chimps than to
gorillas?
>
> What is John's premise in the above comparisons? That DNA sequences
> that are alike mean relationship. He chooses 76 nucleotides that make
> some "claim," as he puts it. The claim, I take it, is that these
> sequences are unique to both humans and chimps. Armed with this
> similarity, and the faulty premise that similarity must mean
> relationship, he proceeds to show how much more similar the
> human/chimp relationships are than any other primate.
>
This is a meaning of "unique" which I have not previously encountered. The
sequences are found in both humans and other apes; homologues are probably
found in monkeys as well, and it would not surprise me to find them in many
other mammalian species.
>
> Well, big whoopdeedoo.
>
> I can decide that similarity between computer-generated characters
> means that they are related, too. I can point out where the
> similarities lie, and how much more similar certain computer-generated
> characters are than others. That does not make the characters any
> more related to each other, just by my setting up some unsupported
> standard that says similarity means relationship.
>
> First John needs to establish the validity of his premise, that
> similarity HAS to mean relationship. He has not done so.
>
Or you have not understood his argument.
>
> snip>
>
-- Steven J.
Zoe
<sjt195...@nts.link.net.INVALID> wrote:
>
>"Zoe" <muz...@aol.com> wrote in message
>news:io8ge1da66g48bj0b...@4ax.com...
>> On Mon, 25 Jul 2005 01:33:57 -0500, "Steven J."
>> <sjt195...@nts.link.net.INVALID> wrote:
>>
>-- [snip]
>>
>> the problem is not with the number of assumptions. It is with the
>> fact that parsimony is applied to a situation in which numbers are
>> irrelevant. Random mutations have no order governing them. They can
>> happen often or little or not at all, according to sheer dumb luck, as
>> you put it. So to try to apply a principle of order and "how it
>> should be" to random activity would be useless, I think.
>>
>Zoe, if your statements above were true, why would there be -- how *could*
>there be -- such a thing as a "mutation rate?" For that matter, how could
>there be "hot spots" on chromosomes where mutations are more likely than at
>other loci? "Random," with respect to mutations, does not mean that the
>mutations occur for no reason, or that all mutations are equally likely, or
>that there is no possibility of saying how likely a mutation is to occur.
>It means simply that the causes of the mutations, and the causes that make
>some traits beneficial and others harmful, are not related to one another.
>
>For that matter, again, if random events had no order governing them, then
>probability as a field of mathematics could not exist. Your position as
>stated above is pure obstinant folly.
probability and statistics does not explain how a cardboard box is put
together. Neither does it explain how a certain number of chromosomes
are consistently found in any particular life form. It merely
predicts the chances of a single, discrete action occurring. These
threads have had to do with how systems are put together.
So now, are you saying that random events are credited with pulling
together a digestive system or a circulatory system or a cardboard
box? Or are you taking a fully-formed reproductive system and
applying your evolutionary theory of mutations to it? I am really
interested in the construction of the system, not in the mutations
that can happen to the construction.
>>
>-- [snip]
>>
>> if sequence similarity between genes were truly 99.75%, then
>> morphologically, we would be 99.75% similar to chimps. Reality is, we
>> are not 99.75% similar to chimps in our outward appearance. Outward
>> appearance is a result of those same genes that are considered to be
>> almost identical to chimps.
>>
>There is no one-to-one mapping between genotype and phenotype.
I didn't mean genotype and phenotype here, but a one-to-one mapping
between genes and morophology. A specific gene will always produce
the same specific protein or proteins, and if there is another gene
that is identical to it, that identical gene will also produce the
same results. So if the claim is that gene similarity was 99.75%
between chimps and humans, you would expect to find 99.75% similar
morphology.
> A tiny
>alteration in a gene can have an immense effect on how the organism
>develops, or, conversely, very large changes in multiple genes can have no
>effect at all.
references, please, for the claim that large changes in multiple genes
can have no effect at all.
> It has been known for a long time (since well before the
>discovery of genes) that tiny changes in developmental rates (e.g. how long
>a particular structure continues to grow) can produce immense differences in
>how an organism looks -- and tiny changes in development rates can result
>from tiny changes in genes. OTOH, as noted, large sections of many proteins
>(and hence the genes that code for them) can be replaced with completely
>different sequences without affecting function.
references, please?
> Consider how many genetic
>disorders are the result of changing one amino acid in one protein (the
>result of changing one nucleotide in one gene). Equally drastic effects
>that are not disorders can be produced by equally small changes.
examples of these equally drastic effects that are not disorders?
>>
>>> Note that the authors distinguish between "adaptive
>>>evolution" ("beneficial mutations") and, presumably, evolution that isn't
>>>adaptive. If I'm reading this right, about 83% of the genes show *some*
>>>difference (perhaps only one or two nucleotides altered), and about 3% of
>>>genes show differences that resulted from beneficial mutations spreading
>>>through natural selection, and the rest show differences that are inferred
>>>to have arisen through neutral mutations that drifted to fixation. Of
>>>course, this summary does not enable me to determine how they decided
>>>which
>>>changes were adaptive and which were not.
>>
>> is there even a way to determine if a change is adaptive versus a
>> result of some rare "beneficial" mutation?
>>
>"Beneficial" mutations are by definition "adaptive," since both "beneficial"
>and "adaption" are diagnosed because they enhance the organism's chances of
>surviving and reproducing in a particular environment. Not all adaptive
>change is the result of mutations: it may be that the "fitter" or better
>adapted alleles are already present in the population, and simply become
>more common due to natural selection. "Adaptive" evolution simply means
>that alleles that are more beneficial become more common, whether those
>alleles arise from new mutations or have been present since the parent
>population first evolved.
so how do you determine whether an adaptation is inherent or a result
of beneficial mutations? You haven't answered that yet.
you're excluding yourself, Steven? :-)
> would infer that one of those two sentences was the original, and
>the other was derived by either adding or removing the initial "not."
I did not assume that one of the two sentences was an original. In
the creationist worldview, one sentence could be original to them. In
the evolutionist worldview, the other sentence could be original to
them. They are simply original statements of belief, neither copying
the other.
>-- [snip]
>>
>> a nested hierarchy would only be strong evidence if there are no other
>> nested hierarchies that form in the real world. To ignore the fact
>> that there are other nested hierarchies in the real world that are not
>> a result of common descent, and then claim that this one particular
>> nested hierarchy must be the result of common descent, is to impose an
>> undue burden upon the one evolutionary hierarchy.
>>
>Strictly speaking, one can arrange any set of entities in a nested
>hierarchy.
which is what has been done for the biological world. Humans have
arranged biological life forms into hierarchies.
> Anyone who's ever written an outline for a paper, or tried to
>sort books in a library, has arranged ideas or objects in a nested
>hierarchy. Note, though, that for many sets of objects, there are multiple
>equally valid hierarchical arrangements of the objects. A book on, e.g.
>_The History of the Spread of the Great Plague_ might be filed under
>"History," or "Epidemiology," or "Diseases." One can arrange automobiles in
>many different nested hierarchies: arrange them by manufacturer (e.g. GM
>cars, and within that category Dodges, Cadillacs, Chevrolets, etc.), or by
>type of vehicle (e.g. sedans, and under sedans GM sedans, Ford sedans,
>etc.), or by various other schemes. One can always get a nested hierarchy,
>but the hierarchy one gets depends on the traits one selects to compare.
and the traits selected for biology is morphology and genetics, right?
Biology can also be classified into other hierarchies, using other
traits as standards, such as habits, location, size, mental abilities,
and so on.
All that hierarchies demonstrate is the ability of humans to
categorize and compare.
>What makes biology interesting is that one can pick many different sets of
>traits to compare, and get the *same* nested hierarchy.
as long as you are consistently categorizing the same items, whether
books or cars or life forms, you will always get nested hierarchies
for whatever traits are chosen to be used as a categorizing tool. For
any category chosen, you WILL get the same nested hierarchy because
you are dealing with the same category of things.
> The most-cited
>example is the hierarchy formed by comparison of anatomical features and
>that formed by comparing genes and proteins (the "twin nested hierarchy),
don't stop at "twin nested". You can get triple nested, too, or
quadruple nested. The ability to categorize in a hierarchical manner
doesn't demonstrate much, other than the ability to compare, since
anything else can be formed into several nested hierarchies, also.
>but one can see the same thing just be comparing, say, anatomical features.
>All organisms with one bone in the lower jaw and three in the middle ear
>also have mammary glands, and none have feathers. There's no obvious
>reason, assuming separate origins, for that feature -- why not bats with
>feathers, or penguins with mammary glands? *Consistent* nested hierarchies
>do not arise through known methods of design -- human engineers cross-copy
>components into very different designs (e.g. CD players installed in both GM
>sedans and Ford trucks). Nature does not: pterosaurs and bats, although
>both used furry membranous wings, use different ways of modifying forelimbs
>to produce those wings.
are you saying that similarity, wherever observed, must always be
evidence of common roots and never evidence of cross-copying? On what
basis do you decide that certain similarities cannot be the result of
cross copying and other similarities are the result of cross-copying?
I hope the basis isn't that: "There is no mind higher than ours,
therefore anything that has no human creator must be self created from
a common root."
>> For the evolutionary understanding of nested hierarchy, see:
>>
>> http://www.lobue.com/enterprise_evolution/knowledge_hierarchy.html
>>
>This is astonishing. You may just have found the worst explanation of what
>evolutionists mean by "nested hierarchy" on the entire World Wide Web (this
>is not to say that the explanation is useless for other purposes). I would
>suggest, rather,
>
>http://www.talkorigins.org/faqs/comdesc/CDhierarchy.html
>http://www.talkorigins.org/faqs/comdesc/CDhierarchy.html
same link
>http://www.isss.org/hierarchy.htm
these links say, just in detail, what my link says in brief. I
understand that nested hierarchies can be developed for just about
anything, and that includes biological life forms.
>> by the above evolutionary admission, there are other nested
>> hierarchies besides the biological hierarchies.
>>
>> Nested hierarchy is just another term for levels of organization. You
>> find levels of organization in many other fields besides biology.
>> None of these other fields draw the conclusion that, therefore, common
>> source or ancestry is indicated.
>>
>Actually, a "nested" hierarchy has not merely levels of organization, but
>the lower levels form parts of the higher levels, as, e.g. "primates" are
>part of the "mammals," which are part of the "vertebrates."
agreed, if these are the classification standards chosen.
>> Take, for instance, the following hierarchy for all humans.
>>
>> Using geographical boundaries. North America: USA: Florida: Seminole
>> County: Orlando: 100 East Street: Human: John Doe.
>>
>John Doe is not a geographical feature; he is not part of East Street, or
>part of the geography of Seminole County. Note, furthermore, that [a] if
>John Doe moves to California, he ceases to be part of Seminole County in any
>sense, and [b] John Doe can, as you note below, be classified as part of a
>quite different nested hierarchy. Again, you are ignoring the salient and
>compelling nature of the consistent nested hierarchies in biology.
I expect any nested hierarchy to be consistent as long as the
categorization is consistently of the same group.
>> Using ecological boundaries. Biome: Community: Population: Human:
>> John Doe.
>>
>> Lo, we have a twin-nested hierarchy.
>>
>No, you have two quite different nested hierarchies containing the same
>entity.
okay, so I'm not the greatest classifier, but it doesn't mean
twin-nested hierarchies cannot be drawn up for just about any set of
things.
> Again, one can construct nested hierarchies for any set of objects
>or ideas, but the distinctive feature of life is that it falls into pretty
>much the same hierarchy no matter what traits one seeks to compare.
actually, this is not a distinctive feature of life. It is a feature
of any group of things one chooses to categorize hierarchically.
snip what has already been answered>
>>>No, neutral drift consists of sheer dumb luck, which is a very different
>>>matter from natural selection. Evolutionary theory encompasses both,
>>>although evolutionists argue among themselves as to which explains more
>>>genetic change over time (hardly anyone disputes that natural selection
>>>explains *adaptive* change, but not all change is adaptive). Note that
>>>sheer dumb luck is quite predictable, which is why Las Vegas casinos
>>>manage
>>>to stay in business, and quite scientific, which is why probability and
>>>statistics exist as branches of mathematics.
>>
>> probability and statistics has nothing to do with organization and
>> building and creating. It just says what are the chances of something
>> happening. Once the thing happens, probability and statistics can
>> only say what are the chances that such a thing can happen again. You
>> don't use probability and statistics to build something in an orderly
>> and methodical manner.
>>
>Some orderly systems do, in fact, arise from purely stochastic processes,
>but that is not my point.
>>
>> Explain to me how you build a digestive system via the mechanism of
>> blind, sheer dumb luck. Or make it easier. Explain how you would
>> build a cardboard box via the mechanism of sheer dumb luck.
>>
>I have distinguished between adaptive evolution (which I attribute to
>natural selection of mutations), and nonadaptive evolution, which I have
>attributed largely to genetic drift ("dumb luck"). Digestive systems are
>adaptions. Please try harder to understand the arguments directed at you.
please, Steven, dearest, try harder to understand my question, which
is, again:
Explain to me how you build a digestive system via the mechanism of
blind, sheer dumb luck. Or make it easier. Explain how you would
build a cardboard box via the mechanism of sheer dumb luck.
snip>
>When you are prepared to think about the arguments presented to you, we can
>continue.
I've thought about the arguments, find them unpersuasive, so I shall
indeed continue on....to Creation Theory-6. :-)
Steven J.
> On Wed, 27 Jul 2005 23:54:26 -0500, "Steven J."
> <sjt195...@nts.link.net.INVALID> wrote:
>
>
>>For that matter, again, if random events had no order governing them, then
>>probability as a field of mathematics could not exist. Your position as
>>stated above is pure obstinant folly.
>
> probability and statistics does not explain how a cardboard box is put
> together. Neither does it explain how a certain number of chromosomes
> are consistently found in any particular life form. It merely
> predicts the chances of a single, discrete action occurring. These
> threads have had to do with how systems are put together.
>
chromosomes" is not found consistently in any particular species; there are
species with varying numbers of chromosomes in different individuals.
Heredity explains (to the extent that heredity is understood) why, in
general, chromosome counts don't vary wildly from parent to offspring or
individual to individual within a species.
>
> So now, are you saying that random events are credited with pulling
> together a digestive system or a circulatory system or a cardboard
> box? Or are you taking a fully-formed reproductive system and
> applying your evolutionary theory of mutations to it? I am really
> interested in the construction of the system, not in the mutations
> that can happen to the construction.
>
digestive system (at least, not by themselves); random events in combination
with natural selection (reproduction, variation, and differential
reproductive success) put complex structures together.
>
>>>
>>-- [snip]
>>>
>>> if sequence similarity between genes were truly 99.75%, then
>>> morphologically, we would be 99.75% similar to chimps. Reality is, we
>>> are not 99.75% similar to chimps in our outward appearance. Outward
>>> appearance is a result of those same genes that are considered to be
>>> almost identical to chimps.
>>>
>>There is no one-to-one mapping between genotype and phenotype.
>
> I didn't mean genotype and phenotype here, but a one-to-one mapping
> between genes and morophology. A specific gene will always produce
> the same specific protein or proteins, and if there is another gene
> that is identical to it, that identical gene will also produce the
> same results. So if the claim is that gene similarity was 99.75%
> between chimps and humans, you would expect to find 99.75% similar
> morphology.
>
"morphology?" Now, to be sure, to a biologist "phenotype" includes behavior
(a pointer's tendency to point at birds is as much part of its phenotype as
the shape of its ears), and may even include results of that behavior
(Richard Dawkins has argued for treating, e.g. beaver dams and termite
mounds as part of the phenotypes of these species), but it's basically "what
the genes build, directly or indirectly, in a given environment."
http://w3.fiu.edu/milesk/genetics.htm
Let's take a simple case and question: are chihuahuas and St. Bernards 99+%
similar in morphology (note that not merely size, but proportions and even
toe number may vary between these breeds)? Domestic dogs differ from grey
wolves by only about 0.2% of their mitochrondrial DNA (and mitochrondrial
DNA mutates faster and is more variable than nuclear DNA, which is what we
were comparing with humans and chimps above), so the degree of genetic
difference between any two dog breeds must be very tiny indeed. I'm not
sure how you'd quantify the difference between, e.g. the St. Bernard and the
chihuahua, or a greyhound and a dachsund, but I think you'd easily come up
with less than 99.9% similarity in appearance, for all that their genetic
similarity can be that great.
>
>> A tiny
>>alteration in a gene can have an immense effect on how the organism
>>develops, or, conversely, very large changes in multiple genes can have no
>>effect at all.
>
> references, please, for the claim that large changes in multiple genes
> can have no effect at all.
>
http://globin.cse.psu.edu/html/huisman/variants/contents.html
There are over 1000 documented variants in human hemoglobin. Granted, many
of these produce very marked and generally deleterious phenotypic effects
(e.g. sickle-cell anemia, thalassemia, etc.), but others have no apparent
difference in function from normal human hemoglobin. Or consider this:
there is a gene, Pax-6, which triggers eye development in fruit flies.
Humans also have a form of Pax-6 (which controls development of the iris of
the human eye), which is not identical to the fruit fly version, but
experimenters have induced fruit fly eyes to grow on fruit fly wings by
introducing *human* Pax-6 genes into the wings (there are, of course,
already fruit fly Pax-6 genes in the wings, but they are deactivated).
Evidently, fruit flies could develop normally if some of their genes were
replaced by their human homologues, which implies, again, that large changes
in multiple genes could have little or no noticeable effect. The large
variations in sequence between cytochrome-c in various species, together
with the similarity in function of the enzyme in different species, likewise
suggests that changes in genes don't map one-to-one directly to changes in
morphology or behavior.
>
>> It has been known for a long time (since well before the
>>discovery of genes) that tiny changes in developmental rates (e.g. how
>>long
>>a particular structure continues to grow) can produce immense differences
>>in
>>how an organism looks -- and tiny changes in development rates can result
>>from tiny changes in genes. OTOH, as noted, large sections of many
>>proteins
>>(and hence the genes that code for them) can be replaced with completely
>>different sequences without affecting function.
>
> references, please?
>
The classic examples of small changes in genes producing large phenotypic
effects are things like four-winged fruit flies (the rear wings are produced
by a single mutation modifying the growth of the halteres behind the
front -- and in normal flies, only -- wings), or achondroplasty in humans or
dogs (a mutation that shortens the limbs).
It is well-known that some homologous proteins between different species are
very different in sequence (e.g. the aforementioned cytochrome-c, or the
even more widely varying fibrins, while others (e.g. the histones that form
the backbones of chromosomes) differ very little between species. And I've
mentioned that there are variants in hemoglobin within the human species,
some of which don't seem to have much in the way of effects. The inference,
of course, is that nearly all alterations to histones prevent them from
working properly, while hemoglobin and cytochrome-c can vary much more
without affecting function.
http://alpha2.bmc.uu.se/~lars/biowww/Proteinevol.html
>
>> Consider how many genetic
>>disorders are the result of changing one amino acid in one protein (the
>>result of changing one nucleotide in one gene). Equally drastic effects
>>that are not disorders can be produced by equally small changes.
>
> examples of these equally drastic effects that are not disorders?
>
Does
http://www.hindu.com/thehindu/seta/2002/03/07/stories/2002030700060300.htm
count? It involves a mutation that drastically reduces the number of pairs
of legs in a species of shrimp, without so far as I can tell actually
crippling the shrimp.
http://www.talkorigins.org/faqs/mutations.html#Q2 has a list of favorable
mutations in various species, which would certainly seem to answer your
request.
You weren't asking that question. With bacteria or fruit flies, watching
evolution in real time, one can sequence individuals at the start and end of
the experiment and spot the mutations. In the case of humans and chimps,
one can only note that certain alleles that are ubiquitous in humans are
unknown in chimps, and infer that either humans or chimps have experienced a
mutation since the LCA.
>
-- [snip example of difference between Zoe logic and Earth logic]
But pretty clearly ear bones and mammary glands are not the same things.
Having hair and having a single (left) aortic arch (as opposed to having two
aortic arches like many reptiles, or a single right arch like birds) are not
the same thing either. So why, if you create a category of all vertebrates
that have three bones in the inner ear, have you also, automatically,
created a category of all vertebrates with mammary glands, a single left
aortic arch, and fur?
If I create a category of all cars with automatic transmissions and four
doors, that will not the the same as, or entirely contain, or be entirely
contained within, a category of, e.g. "all Ford cars with CD players."
Consistent nested hierarchies which arise independently from comparisons of
many different sets of traits are not found in designed artifacts.
>
>> The most-cited
>>example is the hierarchy formed by comparison of anatomical features and
>>that formed by comparing genes and proteins (the "twin nested hierarchy),
>
> don't stop at "twin nested". You can get triple nested, too, or
> quadruple nested. The ability to categorize in a hierarchical manner
> doesn't demonstrate much, other than the ability to compare, since
> anything else can be formed into several nested hierarchies, also.
>
The point, again, is that living things fall into *one* nested hierarchy,
regardless of the features chosen in order to arrange that hierarchy. That
is a product of branching descent with inheritance and modification, and
only of such a process.
>
>>but one can see the same thing just be comparing, say, anatomical
>>features.
>>All organisms with one bone in the lower jaw and three in the middle ear
>>also have mammary glands, and none have feathers. There's no obvious
>>reason, assuming separate origins, for that feature -- why not bats with
>>feathers, or penguins with mammary glands? *Consistent* nested
>>hierarchies
>>do not arise through known methods of design -- human engineers cross-copy
>>components into very different designs (e.g. CD players installed in both
>>GM
>>sedans and Ford trucks). Nature does not: pterosaurs and bats, although
>>both used furry membranous wings, use different ways of modifying
>>forelimbs
>>to produce those wings.
>
> are you saying that similarity, wherever observed, must always be
> evidence of common roots and never evidence of cross-copying? On what
> basis do you decide that certain similarities cannot be the result of
> cross copying and other similarities are the result of cross-copying?
>
I was talking, in this case, about *dissimilarity*. Pterosaurs and bats
clearly aren't examples of cross-copying, because their shared features are
all shared with the larger category of amniote vertebrates, and their
derived features -- e.g. wings and other flight adaptions -- are different
from each other. Just as a tape player in one truck isn't cross-copied from
a CD player in another, so bird, bat, and pterosaur wings don't seem to be
examples of cross-copying. Conversely, we see that small, insect-eating
birds have the same basic wing structure as large birds like eagles (or
ostriches, for that matter), while small, insect-eating bats have the same
basic wing structure (as well as many other anatomical similarities to)
large fruit bats. If wings aren't cross-copied between bats and birds in
similar ecological niches, and both bats and birds fall into the consistent
nested hierarchies expected from common descent, isn't it reasonable to
ascribe the shared wings of bats to common roots? Indeed, the various
creationists who speak of a "bat kind" seem to accept this reasoning.
>
-- [snip]
>
-- Steven J.
John Harshman
I'm afraid all that is irrelevant, since we're not talking about
aneuploidy (which is what the snippet is discussing), but fusions.
Karyotyping can tell you whether the offspring has inherited the unfused
state from one parent and the fused state from another.
>>>>The factors that allow or prevent interbreeding are complex,
>>>>but simple length of time apart is one of them.
>>>
>>>
>>>so would your theory predict that the Chinese race, living apart from
>>>the Indian race, would eventually, over time, evolve the inability to
>>>interbreed?
>>
>>If that were true, then yes it would. However, no human population has
>>ever been that isolated. There is no Chinese race and no Indian race,
>>just clinal variation from one point to another.
>
> my point was, according to evolutionary ideas, if there are groups of
> Chinese that have never been to India, and groups of Indians that
> never went to China, would members of those particular groups, should
> they ever meet after thousands of years, be unable to interbreed?
>
> snip the rest of John's non-answers>
It wasn't a non-answer. Read it and try to understand. It doesn't matter
whether anyone travels between China and India, as long as there is a
chain of interbreeding populations in between -- which there is. What
you may have been trying to say, and it's hard to tell, is that if there
were total isolation between China and India for a long enough period,
the inhabitants would become different species. And that's true, though
how much time would be required is unclear.
ErikW
No. If he were to type out all nucleotide positions in that sequence it
would take too much space. So he excluded all nucleotides that are not
different between all species because they don't make any claim about
relationships. (That they make no claim means that they are not
informative, i.e. have no information to contribute to this particular
question.) What remains after pruning out nucleotide positions that do
not make any claim are those that contain differences that are shared
between two or more species in the table since they have the necessary
information. The claims that the postitions make are different for
different positions and he included all of them. (It's all written in
the quote you presented above. I got the impression that you
misunderstood it, however.)
> Armed with this
> similarity, and the faulty premise that similarity must mean
> relationship, he proceeds to show how much more similar the
> human/chimp relationships are than any other primate.
>
> Well, big whoopdeedoo.
You might want to consider another claim of his from that post: "By
itself, this is pretty good evidence for the African ape connection.
But if I did this little exercise with any other gene I would get the
same result too."
Something worth thinking about.
Zoe
<sjt195...@nts.link.net.INVALID> wrote:
>
>"Zoe" <muz...@aol.com> wrote in message
>news:igsne1tsdue4nfr1b...@4ax.com...
>> On Wed, 27 Jul 2005 23:54:26 -0500, "Steven J."
>> <sjt195...@nts.link.net.INVALID> wrote:
>>
>-- [snip]
>>
>>>For that matter, again, if random events had no order governing them, then
>>>probability as a field of mathematics could not exist. Your position as
>>>stated above is pure obstinant folly.
>>
>> probability and statistics does not explain how a cardboard box is put
>> together. Neither does it explain how a certain number of chromosomes
>> are consistently found in any particular life form. It merely
>> predicts the chances of a single, discrete action occurring. These
>> threads have had to do with how systems are put together.
>>
>Zoe, I thought that we had established that, in fact, a "certain number of
>chromosomes" is not found consistently in any particular species; there are
>species with varying numbers of chromosomes in different individuals.
>Heredity explains (to the extent that heredity is understood) why, in
>general, chromosome counts don't vary wildly from parent to offspring or
>individual to individual within a species.
Steven, I'm talking about the usefulness of probability and statistics
in explaining how a cardboard box is put together or in determining
how chromosomes are consistently the same for any group of life forms.
It isn't useful for these purposes, is it?
>> So now, are you saying that random events are credited with pulling
>> together a digestive system or a circulatory system or a cardboard
>> box? Or are you taking a fully-formed reproductive system and
>> applying your evolutionary theory of mutations to it? I am really
>> interested in the construction of the system, not in the mutations
>> that can happen to the construction.
>>
>No, I am not saying that random events are credited with putting together a
>digestive system (at least, not by themselves); random events in combination
>with natural selection (reproduction, variation, and differential
>reproductive success) put complex structures together.
and this is the process that has not yet been explained by posters to
TO -- not one. Please describe a scenario, based on facts, not
fantasy, of how a digestive system comes together through random
events in combination with natural selection. And you cannot use
reproduction, variation, and differential reproductive success unless
you are willing to concede that the machinery was already in place,
fully functioning, after which comes along your mutations and
selection.
So, okay, we have a simple common ancestor consisting of a single
functioning cell (and even that is a generous given) that replicates
(we know not how that started). Take it from there and describe a
realistic scenario, using factual, scientific observations, as to how
this single cell develops a digestive system, based on random
mutations and selection.
Can't do it? Then evolutionists need to be a little humbler about
their position. To say "We know the digestive system evolved," but go
silent when the question of "how?" is asked, is to ask thinking minds
to take your word on faith.
So, here we go.
A single cell exists, replicating itself repeatedly. Along comes a
random "beneficial mutation." What happens next, based on your
selection principle? How does the digestive system develop?
>>
>>>>
>>>-- [snip]
>>>>
>>>> if sequence similarity between genes were truly 99.75%, then
>>>> morphologically, we would be 99.75% similar to chimps. Reality is, we
>>>> are not 99.75% similar to chimps in our outward appearance. Outward
>>>> appearance is a result of those same genes that are considered to be
>>>> almost identical to chimps.
>>>>
>>>There is no one-to-one mapping between genotype and phenotype.
>>
>> I didn't mean genotype and phenotype here, but a one-to-one mapping
>> between genes and morophology. A specific gene will always produce
>> the same specific protein or proteins, and if there is another gene
>> that is identical to it, that identical gene will also produce the
>> same results. So if the claim is that gene similarity was 99.75%
>> between chimps and humans, you would expect to find 99.75% similar
>> morphology.
>>
>What is your definition of "phenotype," and how does "phenotype" differ from
>"morphology?"
phenotype has to do with group characteristics, psychological and
anatomical, resulting from both heredity and environment. It refers
to characteristics of organisms collectively, or a group of organisms
having like characteristics.
Morphology has to do with individual characteristics, the form and
structure of individual animals and plants.
>Now, to be sure, to a biologist "phenotype" includes behavior
>(a pointer's tendency to point at birds is as much part of its phenotype as
>the shape of its ears), and may even include results of that behavior
>(Richard Dawkins has argued for treating, e.g. beaver dams and termite
>mounds as part of the phenotypes of these species), but it's basically "what
>the genes build, directly or indirectly, in a given environment."
>
>http://w3.fiu.edu/milesk/genetics.htm
>
>Let's take a simple case and question: are chihuahuas and St. Bernards 99+%
>similar in morphology (note that not merely size, but proportions and even
>toe number may vary between these breeds)? Domestic dogs differ from grey
>wolves by only about 0.2% of their mitochrondrial DNA (and mitochrondrial
>DNA mutates faster and is more variable than nuclear DNA, which is what we
>were comparing with humans and chimps above), so the degree of genetic
>difference between any two dog breeds must be very tiny indeed. I'm not
>sure how you'd quantify the difference between, e.g. the St. Bernard and the
>chihuahua, or a greyhound and a dachsund, but I think you'd easily come up
>with less than 99.9% similarity in appearance, for all that their genetic
>similarity can be that great.
nuclear DNA produces morphological similarity. MtDNA has to do with
energy transfer, not morphological similarities. So why are you using
MtDNA as an example of morphological similarity?
>>> A tiny
>>>alteration in a gene can have an immense effect on how the organism
>>>develops, or, conversely, very large changes in multiple genes can have no
>>>effect at all.
>>
>> references, please, for the claim that large changes in multiple genes
>> can have no effect at all.
>>
>http://globin.cse.psu.edu/html/huisman/variants/contents.html
want to summarize or quote the section from this that describes very
large changes in multiple genes having no effect at all? Giving me
this link is tantamount to someone asking me a Biblical question and I
throw the whole Bible at them and say, "there's your reference."
>There are over 1000 documented variants in human hemoglobin. Granted, many
>of these produce very marked and generally deleterious phenotypic effects
>(e.g. sickle-cell anemia, thalassemia, etc.), but others have no apparent
>difference in function from normal human hemoglobin.
reference and quote, please? Not the whole library, but something
specific that you have read in the above.
> Or consider this:
>there is a gene, Pax-6, which triggers eye development in fruit flies.
>Humans also have a form of Pax-6 (which controls development of the iris of
>the human eye), which is not identical to the fruit fly version, but
>experimenters have induced fruit fly eyes to grow on fruit fly wings by
>introducing *human* Pax-6 genes into the wings (there are, of course,
>already fruit fly Pax-6 genes in the wings, but they are deactivated).
>Evidently, fruit flies could develop normally if some of their genes were
>replaced by their human homologues, which implies, again, that large changes
>in multiple genes could have little or no noticeable effect.
I don't know how you can draw such a sweeping conclusion from an
experiment that shows that fruit fly eyes can grow on fruit fly wings.
Until you present fruit flies that are reproducing successfully with
eyes on their wings, how can you say that there is no apparent
difference in function with these changes?
> The large
>variations in sequence between cytochrome-c in various species, together
>with the similarity in function of the enzyme in different species, likewise
>suggests that changes in genes don't map one-to-one directly to changes in
>morphology or behavior.
first of all, you need to demonstrate that these variations in
sequence are really a result of changes over time and not a result of
original makeup. It's like an ant looking at the differences between
a car and a plane and saying, "see these differences? They are a
result of changes that occurred over millions of years." A second ant
says, "how can you tell this?" The first ant says, "because, can't
you see that changes occur as a normal course of events? See here,
rust builds up on this car, and the fender falls off eventually.
Therefore, given enough time, the car will end up being a plane."
>>> It has been known for a long time (since well before the
>>>discovery of genes) that tiny changes in developmental rates (e.g. how
>>>long
>>>a particular structure continues to grow) can produce immense differences
>>>in
>>>how an organism looks -- and tiny changes in development rates can result
>>>from tiny changes in genes. OTOH, as noted, large sections of many
>>>proteins
>>>(and hence the genes that code for them) can be replaced with completely
>>>different sequences without affecting function.
>>
>> references, please?
>>
>The classic examples of small changes in genes producing large phenotypic
>effects are things like four-winged fruit flies (the rear wings are produced
>by a single mutation modifying the growth of the halteres behind the
>front -- and in normal flies, only -- wings), or achondroplasty in humans or
>dogs (a mutation that shortens the limbs).
and these four-winged fruit flies, do they reproduce successfully?
>It is well-known that some homologous proteins between different species are
>very different in sequence (e.g. the aforementioned cytochrome-c, or the
>even more widely varying fibrins, while others (e.g. the histones that form
>the backbones of chromosomes) differ very little between species. And I've
>mentioned that there are variants in hemoglobin within the human species,
>some of which don't seem to have much in the way of effects. The inference,
>of course, is that nearly all alterations to histones prevent them from
>working properly, while hemoglobin and cytochrome-c can vary much more
>without affecting function.
>
>http://alpha2.bmc.uu.se/~lars/biowww/Proteinevol.html
the mistake made here is to assume that differences in sequence arose
as a result of external mutational change instead of recognizing that
beneficial differences were there from the beginning.
>>> Consider how many genetic
>>>disorders are the result of changing one amino acid in one protein (the
>>>result of changing one nucleotide in one gene). Equally drastic effects
>>>that are not disorders can be produced by equally small changes.
>>
>> examples of these equally drastic effects that are not disorders?
>>
>Does
>http://www.hindu.com/thehindu/seta/2002/03/07/stories/2002030700060300.htm
>count? It involves a mutation that drastically reduces the number of pairs
>of legs in a species of shrimp, without so far as I can tell actually
>crippling the shrimp.
so humans have learned how to manipulate the Hox gene to create
changes. One point for intelligence. How does this support
evolution? Indeed, do you have evidence that these fruit flies and
shrimp can successfully reproduce after their genes have been
manipulated to stop limb development?
>http://www.talkorigins.org/faqs/mutations.html#Q2 has a list of favorable
>mutations in various species, which would certainly seem to answer your
>request.
please, not the same old tired list of six examples. In any event,
what you call favorable mutations, I call inherent ability to vary or
adapt to environmental stimuli. How are we going to demonstrate which
is correct? I'm betting there is no predictability test or
explanatory test that will demonstrate that these responses to the
environment are really favorable mutations from the outside. However,
creation theory would predict that favorable adjustments to
environmental stimuli (what you call favorable mutations) can be
traced to an internal program that allows for such variations.
snip>
>> so how do you determine whether an adaptation is inherent or a result
>> of beneficial mutations? You haven't answered that yet.
>>
>You weren't asking that question.
I thought I was.
> With bacteria or fruit flies, watching
>evolution in real time, one can sequence individuals at the start and end of
>the experiment and spot the mutations.
and how do you determine that what you are observing are mutations
from the outside or inherent ability to vary, coming from the inside
of the genetic system?
It's like watching figures morph in a computer program and claiming
that the changes are a result of random external mutations when, all
along, the ability to change was programmed into the morphing figures.
Have you tracked the source of these changes to determine if they are
external or internal?
> In the case of humans and chimps,
>one can only note that certain alleles that are ubiquitous in humans are
>unknown in chimps, and infer that either humans or chimps have experienced a
>mutation since the LCA.
see, you're basing your conclusions on a preconceived notion that any
differences have to be a result of change over time from some LCA.
There is no evidence for this other than a just-so story. Since the
faulty premise is that change is always a sign of mutations, then when
something that was built to change, changes, the conclusion is that,
see, mutations did it. The problem is with the premise.
snip>
>> as long as you are consistently categorizing the same items, whether
>> books or cars or life forms, you will always get nested hierarchies
>> for whatever traits are chosen to be used as a categorizing tool. For
>> any category chosen, you WILL get the same nested hierarchy because
>> you are dealing with the same category of things.
>>
>But pretty clearly ear bones and mammary glands are not the same things.
>Having hair and having a single (left) aortic arch (as opposed to having two
>aortic arches like many reptiles, or a single right arch like birds) are not
>the same thing either. So why, if you create a category of all vertebrates
>that have three bones in the inner ear, have you also, automatically,
>created a category of all vertebrates with mammary glands, a single left
>aortic arch, and fur?
doesn't mean a thing. Why, if I create a category of all cars that
have four doors, don't I also automatically create a category of all
cars with windshields, a steering wheel, and wheels?
>If I create a category of all cars with automatic transmissions and four
>doors, that will not the the same as, or entirely contain, or be entirely
>contained within, a category of, e.g. "all Ford cars with CD players."
because you have created a category that doesn't fit, is all. If I
create a category of all vertebrates with three bones in the inner
ear, it will not be in the same category as vertebrates with wings and
beaks.
It's all subjective.
>Consistent nested hierarchies which arise independently from comparisons of
>many different sets of traits are not found in designed artifacts.
I can make them consistent if I choose the right qualities. It's
subjective.
snip more of the same>
>>>but one can see the same thing just be comparing, say, anatomical
>>>features.
>>>All organisms with one bone in the lower jaw and three in the middle ear
>>>also have mammary glands, and none have feathers. There's no obvious
>>>reason, assuming separate origins, for that feature -- why not bats with
>>>feathers, or penguins with mammary glands? *Consistent* nested
>>>hierarchies
>>>do not arise through known methods of design -- human engineers cross-copy
>>>components into very different designs (e.g. CD players installed in both
>>>GM
>>>sedans and Ford trucks). Nature does not: pterosaurs and bats, although
>>>both used furry membranous wings, use different ways of modifying
>>>forelimbs
>>>to produce those wings.
>>
>> are you saying that similarity, wherever observed, must always be
>> evidence of common roots and never evidence of cross-copying? On what
>> basis do you decide that certain similarities cannot be the result of
>> cross copying and other similarities are the result of cross-copying?
>>
>I was talking, in this case, about *dissimilarity*.
you're not answering my question, you know. Why is similarity
evidence of common roots only and never evidence of cross-copying?
> Pterosaurs and bats
>clearly aren't examples of cross-copying, because their shared features are
>all shared with the larger category of amniote vertebrates, and their
>derived features -- e.g. wings and other flight adaptions -- are different
>from each other. Just as a tape player in one truck isn't cross-copied from
>a CD player in another, so bird, bat, and pterosaur wings don't seem to be
>examples of cross-copying.
yet the same intelligence can choose to make a tape and make a CD
player, right?
> Conversely, we see that small, insect-eating
>birds have the same basic wing structure as large birds like eagles (or
>ostriches, for that matter), while small, insect-eating bats have the same
>basic wing structure (as well as many other anatomical similarities to)
>large fruit bats. If wings aren't cross-copied between bats and birds in
>similar ecological niches, and both bats and birds fall into the consistent
>nested hierarchies expected from common descent, isn't it reasonable to
>ascribe the shared wings of bats to common roots?
only if the starting premise is validated that similarity always means
relationship and common roots. You have to establish that premise on
a firm foundation of facts. What facts do you have that will
establish a fundamental rule that similarity always means common
descent or common roots? And if there are exceptions, then on what
basis do you decide that certain similarities mean common root and
other similarities don't?
snip>
Zoe
<jharshman....@pacbell.net> wrote:
and on what basis do you decide that a fusion is inherited versus
formed during meiosis? Were the parents checked and it was found that
one parent had an unfused chromosome and the other had a fused
chromosome? Or is this conclusion drawn only from looking at the
offspring's chromosomes?
snip>
Zoe
<sjt195...@nts.link.net.INVALID> wrote:
it is based on a faulty premise that similarity must mean common
descent or common roots. This premise must be established first. It
has not been. There are too many exceptions where similarity does not
mean common descent to use similarity as evidence of relationship in
the biological world.
>Second, don't you find it rather odd, if the premise of common descent is
>false, that multiple lines of evidence converge on the same phylogeny?
humans can classify just about any group of things so that multiple
lines of similarity (not evidence, btw) would converge.
>Harshman picked a particular set of genes to compare, but one could reach
>the same conclusion by examining other genes, or noncoding DNA sequences, or
>proteins. If all the hominoid (ape + human) species are separately created,
>why do they fall into the sort of pattern we would expect if they were
>produced by braching descent from a common ancestor?
that is the problem. The expectation is misplaced and faulty. I
would expect there to be a pattern in intelligent creation because
that is one of the hallmarks of mental activity -- patterns,
repetition.
> If apes, or some apes,
>are derived by descent with modification from an ape common ancestor, but
>humans are separately created, why do comparisons consistently put humans
>closer to African apes than to Asian apes -- and closer to chimps than to
>gorillas?
whose comparisons are these that put humans closer to African apes
than to Asian apes? John's comparisons? Others with a similar
mindset?
>> What is John's premise in the above comparisons? That DNA sequences
>> that are alike mean relationship. He chooses 76 nucleotides that make
>> some "claim," as he puts it. The claim, I take it, is that these
>> sequences are unique to both humans and chimps. Armed with this
>> similarity, and the faulty premise that similarity must mean
>> relationship, he proceeds to show how much more similar the
>> human/chimp relationships are than any other primate.
>>
>This is a meaning of "unique" which I have not previously encountered. The
>sequences are found in both humans and other apes; homologues are probably
>found in monkeys as well, and it would not surprise me to find them in many
>other mammalian species.
then what claims to relationship do these chosen sequences show, if
not that they are unique? On what basis does John choose 76 sequences
common to humans and chimps, and call them evidence for relationship,
if not similarity?
>> Well, big whoopdeedoo.
>>
>> I can decide that similarity between computer-generated characters
>> means that they are related, too. I can point out where the
>> similarities lie, and how much more similar certain computer-generated
>> characters are than others. That does not make the characters any
>> more related to each other, just by my setting up some unsupported
>> standard that says similarity means relationship.
>>
>> First John needs to establish the validity of his premise, that
>> similarity HAS to mean relationship. He has not done so.
>>
>Or you have not understood his argument.
I think I understand his argument. Can John establish the validity of
his premise, that similarity has to mean relationship?
David Jensen
Zoe <muz...@aol.com> wrote in
<0ns2f1p4dvd74g4fl...@4ax.com>:
Fusions are easily identified.
John Harshman
If a particular fusion is polymorphic within a population, surely it's
much more parsimonious to postulate a single fusion event than a new one
in each individual. Why is this a problem? Your reasoning would make all
genetic studies invalid. Why assume that Queen Victoria was the source
of hemophilia in the royal families of Europe? Couldn't every royal
hemophiliac have been a unique mutant?
John Harshman
> On Thu, 28 Jul 2005 00:08:42 -0500, "Steven J."
> <sjt195...@nts.link.net.INVALID> wrote:
>
>
>>"Zoe" <muz...@aol.com> wrote in message
>>news:aqege1p8ialqf37vs...@4ax.com...
>>
>>>On Mon, 25 Jul 2005 02:11:31 -0500, "Steven J."
>>><sjt195...@nts.link.net.INVALID> wrote:
>>>
>>>
>>>>"Zoe" <muz...@aol.com> wrote in message
>>>>news:6vn8e1h4rfl6ag833...@4ax.com...
[snip]
>>This is a meaning of "unique" which I have not previously encountered. The
>>sequences are found in both humans and other apes; homologues are probably
>>found in monkeys as well, and it would not surprise me to find them in many
>>other mammalian species.
>
>
> then what claims to relationship do these chosen sequences show, if
> not that they are unique? On what basis does John choose 76 sequences
> common to humans and chimps, and call them evidence for relationship,
> if not similarity?
Your near-total confusion is getting in the way big time here. These are
not 76 sequences, but 76 nucleotides from a single pair of genes, ND4
and ND5. These are mitochondrial genes, and in fact homologs are found
in almost all eukaryote species and in many bacteria. The 76 nucleotides
were chosen because they are the informative characters, meaning that
they distinguish one tree from another. The other characters, the
non-informative ones, don't care one little bit what tree they find
themselves on -- most of them are invariant in all the species here, so
tell us nothing at all, and the rest are different in only one species,
and so tell us only that the species is a different species from the
others. The 76 chosen are all the ones that imply some particular tree
out of all the possible trees. The interesting thing is that many more
of them imply an African ape tree than imply any of the other possible
trees. Why should that be? Forget about whether similarity applies
descent for the moment. Just ask yourself why we should see this
particular pattern in the data, and try to explain it. Your idea that
intelligence produces patterns explains nothing, because it is
compatible with any pattern at all. But this particular pattern is what
we expect to see from a branching tree in which African apes are closer
to each other than to all other species. Wouldn't it be a huge
coincidence if, out of all the possible patterns intelligence could have
produced, it just happened to produce the one that fits our evolutionary
theory?
>>>Well, big whoopdeedoo.
>>>
>>>I can decide that similarity between computer-generated characters
>>>means that they are related, too. I can point out where the
>>>similarities lie, and how much more similar certain computer-generated
>>>characters are than others. That does not make the characters any
>>>more related to each other, just by my setting up some unsupported
>>>standard that says similarity means relationship.
>>>
>>>First John needs to establish the validity of his premise, that
>>>similarity HAS to mean relationship. He has not done so.
>>>
>>
>>Or you have not understood his argument.
>
>
> I think I understand his argument.
I think you don't.
> Can John establish the validity of
> his premise, that similarity has to mean relationship?
Don't have to. I just present a pattern, and explain it in the only
obvious way. If you can explain it in some other equally valid way, do
so. If you can't, then we must provisionally accept my explanation. Now
multiply that single case by many thousands of other cases, and you get
a general demonstration of common descent. You don't have to assume that
similarity means relationship. It's a conclusion drawn from the fact
that we see this particular pattern in the data, and we need to come up
with an explanation for it. Common descent is the only one I can come up
with, but you have a go at it.
B Richardson
John Harshman wrote:
Ok, I have about 1002 nucleotides for each of Homo Sapiens,
Gorilla Gorilla, Hyloblates Klossii, Pan Troglodytes and Pongo
Pygmaeus from the same gene. If I post the five sets of nucleotides
can you identify which is which based on the patterns of the
similarities you find?
John Harshman
I could certainly tell you which was Hylobates and which was Pongo. It's
not certain that I could sort out Pan, Homo, and Gorilla, though I would
probably be able to make a guess. 1002 nucleotides is not likely to be
able to resolve that trichotomy.
Why are we performing this exercise?
B Richardson
Thought it might be a different angle for Zoe to look at and help
show her that the idea of relation isn't something that is being
foisted on the data. Dunno, its probably pointless.
John Harshman
Talking to Zoe is almost always pointless. Let's give it a shot.
B Richardson
I will post the sequences in this thread, five posts, one set of
nucleotides per post. I'll leave the subject line untouched. The
first line of each post should read SAMPLE A1, SAMPLE A2, ....
SAMPLE A5. A blank line will follow, then the nucleotides, there
should be nothing else in the posts. I've also trimmed the numbering
on the left side, I was afraid it was getting close to wrapping in
some news readers. There is one each of
Homo sapiens
Pan troglodytes
Gorilla gorilla
Pongo pygmaeus
Hylobates klossii
There is no significance to the sequential scheme A1,A2,A3,A4,A5 and
I've intentionally mixed them up so there would not be.
B Richardson
atgttgactc taactcgcat ccgcactgtg tcctatgaag tcaggagtac atttctgttc
atttcagtcc tggagtttgc agtggggttt ctgaccaatg ccttcgtttt cttggtgaat
ttttgggatg tagtgaagag gcagccactg agcaacagtg attgtgtgct gctgtgtctc
agcatcagcc ggcttttcct gcatggactg ctgttcctga gtgctatcca gcttacccac
ttccagaagt tgagtgaacc actgaaccac agctaccaag ccatcatcat gctatggatg
attgcaaacc aagccaacct ctggcttgct gcctgcctca gcctgcttta ctgctccaag
ctcatccgtt tctctcacac cttcctgatc tgcttggcaa gctgggtctc caggaagatc
tcccagatgc tcctgggtat tattctttgc tcctgcatct gcactgtcct ctgtgtttgg
tgctttttta gcagacctca cttcacagtc acaactgtgc tattcatgaa taacaataca
aggctcaact ggcagattaa agatctcaac ttattttatt cctttctctt ctgctatctg
tggtctgtgc ctcctttcct attgtttctg gtttcttctg ggatgctgac tgtctccctg
ggaaggcaca tgaggacaat gaaggtctat atcagagact ctcgtgaccc cagcctggag
gcccacatta aagccctcaa gtctcttgtc tcctttttct gcttctttgt gatatcatcc
tgtgctgcct tcatctctgt gcccctactg attctgtggc gcgacaaaat aggggtgatg
gtttgtgttg ggataatggc agcttgtccc tctgggcatg cagccgtcct gatctcaggc
aatgccaagt tgaggagagc tgtgacaacc attctgctct gggctcagag cagcctgaag
gtaagagccg accacaaggc agattcccgg acaccgtgct ga
B Richardson
atgttgactc taactcgcat ccgcactgtg tcctatgaag tcaggagtac atttctgttc
atttcagtcc tggagtttgc agtggggttt ctgaccaatg ccttcgtttt cttggtgaat
ttttgggatg tagtgaagag gcaggcactg agcaacagtg attgtgtgct gctgtgtctc
agcatcagcc ggcttttcct gcatggactg ctgttcctga gtgctatcca gcttacccac
ttccagaagt tgagtgaacc actgaaccac agctaccaag ccatcatcat gctatggatg
attgcaaacc aagccaacct ctggcttgct gcctgcctca gcctgcttta ctgctccaag
ctcatccgtt tctctcacac cttcctgatc tgcttggcaa gctgggtctc caggaagatc
tcccagatgc tcctgggtat tattctttgc tcctgcatct gcactgtcct ctgtgtttgg
tgctttttta gcagacctca cttcacagtc acaactgtgc tattcatgaa taacaataca
aggctcaact ggcagaataa agatctcaat ttattttatt cctttctctt ctgctatctg
tggtctgtgc ctcctttcct attgtttctg gtttcttctg ggatgctgac tgtctccctg
ggaaggcaca tgaggacaat gaaggtctat accagaaact ctcgtgaccc cagcctggag
gcccacatta aagccctcaa gtctcttgtc tcctttttct gcttctttgt gatatcatcc
tgtgttgcct tcatctctgt gcccctactg attctgtggc gcgacaaaat aggggtgatg
gtttgtgttg ggataatggc agcttgtccc tctgggcatg cagccatcct gatctcaggc
aatgccaagt tgaggagagc tgtgatgacc attctgctct gggctcagag cagcctgaag
gtaagagccg accacaaggc agattcccgg acactgtgct ga
B Richardson
atgttractc taactcgcat ctgcactgtg tcctatgaag tcaggagtac atttctgttc
atttcagtcc tggagtttgc agtagggttt ctgaccaatg ccttcatttt cttggtgaat
ttttgggacg tagtgaagag gcagccactg agcaacagtg attgtgtgct gctgtgtctc
agcatcagcc ggcttttcct gcatggactg ctgttcctga gtgctatcca gcttacccac
ttccagaagt tgagtgaacc actgaaccac agctaccatg ccatcatcat gctatggatg
attgcaaacc aagccaacct ctggcttgcc acctgcctca gcctgcttta ctgttccaag
ctcatccgtt cctctcacac cttcctgatc tgcttggcaa gctgggtctc caggaagatc
tgccagatgc tcctgggtat tattctttgc tcctgcatct gcactgtcct ctgcgtttgg
tgctatttta gcagacctca cttcacagtc acaactgtgc tattcacgaa taacaataca
aggctcaact ggcagattaa agatctcaac ttattttatt cttttctctt ctgctatctg
tggtctgtgc ctcctttcct attgtttctg gtttcttctg ggatgctgac tgtctccctg
ggaaggcaca tgaggacaat gaaggtctat accagagact tccgtgaccc cagcctggag
gcccacatta aagccctcaa gtctcttgtc tcctttttct gcttctttgt gatatcatcc
tgtgctgcct tcatctcagt gcccctactg attctgtggc gcgacaaaat aggggtaatg
gtttgtgttg ggataatggc agcttgtccc tctgggcatg cagccatcct gatctcaggc
aatgccaagt tgaggagagc tgtgacaacc attctgctct gggctcagag cagtctgaag
B Richardson
atgttgactc taactcgcat ccacactgtg tcctatgaag tcaggagtac atttctgttc
atttcagtcc tggagtttgc agtggggttt ctgaccaatg ccttcgtttt cttggtgaat
ttttgggatg tagtgaagag gcagccactg agcaacagtg attgtgtgct gctgtgtctc
agcatcagcc ggcttttcct gcatggactg ctgttcctga gtgctatcca gcttacccac
ttccagaagt tgagtgaacc actgaaccac agctaccaag ccatcatcat gctatggatg
attgcaaacc aagccaacct ctggcttgct gcctgcctca gcctgcttta ctgctccaag
ctcatccgtt tctctcacac cttcctgatc tgcttggcaa gctgggtctc caggaagatc
tcccagatgc tcctgggtat tattctttgc tcctgcatct gcactgtcct ctgtgtttgg
tgctttttta gcagacctca cttcacagtc acaactgtgc tattcatgaa taacaataca
aggctcaact ggcagattaa agatctcaac ttattttatt cctttctctt ctgctatctg
tggtctgtgc ctcctttcct attgtttctg gtttcttctg ggatgctgac tgtctccctg
ggaaggcaca tgaggacaat gaaggtctat accagagact ctcgtgaccc cagcctggag
gcccacatta aggccctcaa gtctcttgtc tcctttttct gcttctttgt gatatcatcc
tgtgctgcct tcatctctgt gcccctactg attctgtggc gtgacaaaat aggggtgatg
gtttgtgttg ggataatggc agcttgtccc tctgggcatg cagccgtcct gatctcaggc
aatgccaagt tgaggagagc tgtgacgacc attctgctct gggctcagag cagcctgaag
B Richardson
atgttgactc taactcgcat ctgcgctgtg tcctatgaag tcaggagtac atttctgttc
atttcagtcc tggagtttgc agtggggttt ctgaccaatg ccttcatttt cttggtgaat
ttttgggacg tagtgaagag gcagccactg agcaacagtg attgtgtgct gctgtgtctc
agcatcagcc ggcttttcct gcatggactg ctgttcctga gtgctatcca gcttacccac
ttccagaagt tgagtgaacc actgaaccac agctaccaag ccatcatcat gctatrgata
attgcaarcc aagccaacct ctggcttgct gcctgcctca gcctgcttta ctgctccaag
ctcatccgtt tctctcacac cttcctgatc tgcttggcaa gctgggtctc caggaagatc
tcccagatgc ycctgggtat tattctttgc tcctgcatct gcactgtcct ctgtgtttgg
tgctttttta gcagacctca cttcacagtc acaacttttc tattcatgaa taacaataca
aggctcaact ggcagattaa agatctcaac ttattttatt cctttctctt ctgctatctg
tggtctgtgc ctcctttcct attgtttctg gtttcttctg ggatgctgac tgtctccctg
ggaaggcaca tgaggacaat gaaggtctat accagagact ctcgtgaccc cagcctggag
gcccacatta aagccctcaa gtctcttgtc tcctttttct gcttctttgt gatatcatcc
tgtgctgcct tcatctcagt gcccctactg attctgtggc gcaacaaaat aggrgtgatg
gtttgtgttg ggataatggc agcttgtccc tctgggcatg cagctgtcct gatctcaggc
aatgccamrt tgaggagagc tgtgacaacc attctgctct gggctcagag cagcmtgaag
gtaagagccr accacaaggc agattcccgg acactgtgct ga
John Harshman
OK, here are my identifications:
A3 = Hylobates
A5 = Pongo
A1 = Gorilla
A2, A4 = Homo and Pan
Like I said, the first two are easy, the third less clear. And the last
two are interchangeable; there's no possible way to tell them apart just
by the shape of the tree.
Here's how I did this:
First I had to massage slightly to put it into analyzable form using the
program PAUP. I put all the sequences in one text file. I put a _
between SAMPLE and A1, etc., because PAUP recognizes names as everything
before the first space. I added this to the beginning of the file:
#NEXUS
BEGIN DATA;
DIMENSIONS NTAX=5 NCHAR=1002;
FORMAT DATATYPE=DNA ;
MATRIX
The first line reassures PAUP that the file is in its standard format.
The next lines identify a NEXUS data block, tell the program the number
of species and characters, and inform it that the data are DNA. The last
line tells it that the actual data are starting.
Then I added this to the end:
;
end;
Those two lines tell the program that the data are ending, and that the
DATA block is ending.
Then I executed the file in PAUP, which means that I loaded the data
into the program memory, and then did one of the simplest analyses,
neighbor joining. Other methods gave me the same tree. Here's the tree:
Neighbor-joining tree:
/------- SAMPLE A1
| /--------------------------- SAMPLE A2
| /--+------------- SAMPLE A4
\-+ /--------------------[...]------------------- SAMPLE A3
\--------------+------------------------- SAMPLE A5
I had to shorten the branch to A3 so it would fit on this page; that's
what the [...] means. OK, I pick the longest branch, A3 as Hylobates.
Strictly speaking, this only works if there's a uniform rate of
evolution, which is a bad assumption. But usually it will be close
enough to make me confident in my pick. Of course, we will usually have
a designated outgroup in the data, so I wouldn't have to make such a
guess. All else follows from that. The first branch from A3 leads to A5,
so that's Pongo. The next branch leads to A1, so that is suggested to be
Gorilla. Note, however, that the branch separating A1 from A2-A4 is very
short, so it's not very reliable. If A1 is Gorilla, then A2 and A4 are
Homo and Pan, though we can't say which is which.
Anyway, I had only one choice to make, and that was which one is
Hylobates. All else follows from the shape of the tree. Picking
Hylobates requires the single additional assumption that the rate of
evolution doesn't vary too extremely from one species to another.
So, are these more mitochondrial sequences?
B Richardson
> B Richardson wrote:
> > John Harshman wrote:
> >> B Richardson wrote:
> >>> John wrote:
> >>>> B Richardson wrote:
[big snip]
Correct.
> A5 = Pongo
Correct.
> A1 = Gorilla
Correct.
> A2, A4 = Homo and Pan
A2 is Homo, A4 is Pan.
I also had Pan paniscus, I think you would have lock down two Pan
representatives with absolute certainty if I had added it to the mix,
but of course there would have been no way to distinguish between Pan
troglodytes and Pan paniscus.
Thanks for the effort, I find this to have been a noteworthy
excercise.
No, a taste receptor gene. Take note that the Homo entry says
"candidate taste receptor TAS2R38" all the others say
"taste receptor type 2 member 38".
Homo sapiens
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=Nucleotide&dopt=GenBank&val=AF494231
http://tinyurl.com/8cbjg
Gorilla gorilla
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=45549380
http://tinyurl.com/adc6p
Hylobates klossii
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=45549384
http://tinyurl.com/drecx
Pongo pygmaeus
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=45549382
http://tinyurl.com/9bnpu
Pan troglodytes
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=45549378
http://tinyurl.com/7nxco
Pan paniscus
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=45549376
http://tinyurl.com/a6wzw
Charles
with the same topic, but as a layman I find this experiment and its
results illustrative not only of the evidentiary support for evolution,
but how the scientific method works. Therefore, I'd like to nominate
this entire exercise for an August POTM.
Charles
John Harshman
The weird thing is that it evolves so fast. They're evolving faster than
mitochondrial genes in birds. And the transition:transversion bias is
huge, again comparable to bird mt genes. Is this usual for mammalian
protein-coding sequences?
Steve Schaffner
> B Richardson wrote:
>
> > Ok, I have about 1002 nucleotides for each of Homo Sapiens,
> > Gorilla Gorilla, Hyloblates Klossii, Pan Troglodytes and Pongo
> > Pygmaeus from the same gene. If I post the five sets of nucleotides
> > can you identify which is which based on the patterns of the
> > similarities you find?
>
> I could certainly tell you which was Hylobates and which was Pongo. It's
> not certain that I could sort out Pan, Homo, and Gorilla, though I would
> probably be able to make a guess. 1002 nucleotides is not likely to be
> able to resolve that trichotomy.
Also, even if you had enough nucleotides to get a statistically
robust resolution of Pan, Homo and Gorilla, you might well still get
the "wrong" answer. The branching points are close enough that for some
genes, humans really are more closely related to gorillas than to chimpanzees.
--
Steve Schaffner s...@broad.mit.edu
Immediate assurance is an excellent sign of probable lack of
insight into the topic. Josiah Royce
Steven J.
in constructing cardboard boxes, you were talking about random mutations as
though the laws of probability did not apply to them.
>
>>> So now, are you saying that random events are credited with pulling
>>> together a digestive system or a circulatory system or a cardboard
>>> box? Or are you taking a fully-formed reproductive system and
>>> applying your evolutionary theory of mutations to it? I am really
>>> interested in the construction of the system, not in the mutations
>>> that can happen to the construction.
>>>
>>No, I am not saying that random events are credited with putting together
>>a
>>digestive system (at least, not by themselves); random events in
>>combination
>>with natural selection (reproduction, variation, and differential
>>reproductive success) put complex structures together.
>
> and this is the process that has not yet been explained by posters to
> TO -- not one. Please describe a scenario, based on facts, not
> fantasy, of how a digestive system comes together through random
> events in combination with natural selection. And you cannot use
> reproduction, variation, and differential reproductive success unless
> you are willing to concede that the machinery was already in place,
> fully functioning, after which comes along your mutations and
> selection.
>
selective regime, account of how the human digestive tract evolved from a
single-celled organism. I cannot, of course, provide any such thing. I
also suspect that you have neither the intention nor the ability to tell us
how "intelligence" (other, perhaps, than human intelligence) implements any
"design" or change in design in living organisms.
>
> So, okay, we have a simple common ancestor consisting of a single
> functioning cell (and even that is a generous given) that replicates
> (we know not how that started). Take it from there and describe a
> realistic scenario, using factual, scientific observations, as to how
> this single cell develops a digestive system, based on random
> mutations and selection.
>
> Can't do it? Then evolutionists need to be a little humbler about
> their position. To say "We know the digestive system evolved," but go
> silent when the question of "how?" is asked, is to ask thinking minds
> to take your word on faith.
>
happened, without having a complete description of how it happened. Your
position is tantamount to saying that if we can't figure out how someone
died, we are not justified in inferring that he is dead.
You have, in the consistent nested hierarchy of homologies, in biogeography,
in vestigial structures at the genetic and morphological level, in the
fossil record, in the jury-rigged and improvised nature of many adaptions
(e.g. Darwin's remark on "similar structures for dissimilar functions and
dissimilar structures for similar functions"), compelling evidence for
common descent with modification.
You have, furthermore, an demonstrated mechanism of mutation and natural
selection. It has produced, in the lab, bacteria resistant to poisons never
found in nature, bacteria that *eat* poisons never found in nature,
multicellular colonial organisms evolved from single-celled ancestors, and
similar examples of striking novel traits. It seems to me that you are not
being asked to accept anything on "faith," but on the basis of considerable
evidence regarding both the fact and the proposed mechanism for it.
>
> So, here we go.
>
> A single cell exists, replicating itself repeatedly. Along comes a
> random "beneficial mutation." What happens next, based on your
> selection principle? How does the digestive system develop?
>
It becomes a multicellular organism.
http://www.gate.net/~rwms/EvoMutations.html
Starting from single celled animals, each of which has the capability to
reproduce there is no sex in the sense that we think of the term. Selective
pressure has been observed to convert single-cellular forms into
multicellular forms. A case was observed in which a single celled form
changed to multicellularity.
Boxhorn, a student of Boraas,writes:
Coloniality in Chlorella vulgaris
Boraas (1983) reported the induction of multicellularity in a strain of
Chlorella pyrenoidosa (since reclassified as C. vulgaris) by predation. He
was growing the unicellular green alga in the first stage of a two stage
continuous culture system as for food for a flagellate predator, Ochromonas
sp., that was growing in the second stage. Due to the failure of a pump,
flagellates washed back into the first stage. Within five days a colonial
form of the Chlorella appeared. It rapidly came to dominate the culture. The
colony size ranged from 4 cells to 32 cells. Eventually it stabilized at 8
cells. This colonial form has persisted in culture for about a decade. The
new form has been keyed out using a number of algal taxonomic keys. They key
out now as being in the genus Coelosphaerium, which is in a different family
from Chlorella. "
Boraas, M. E. 1983. Predator induced evolution in chemostat culture. EOS.
Transactions of the American Geophysical Union. 64:1102.
There are, of course, an immense number of steps along the way: the
development of multiple layers (starting with something cnidarian-like with
two layers of cells, and gradually evolving (in some lineages) a third
layer), the innermost of which may be devoted to digesting food (note that
the single cell, and its simple colonial descendants, already can take in
food through their surface, so what we are talking about here is having some
fraction of the body cells specialize in a function they already have).
>
-- [snip]
>
>>What is your definition of "phenotype," and how does "phenotype" differ
>>from
>>"morphology?"
>
> phenotype has to do with group characteristics, psychological and
> anatomical, resulting from both heredity and environment. It refers
> to characteristics of organisms collectively, or a group of organisms
> having like characteristics.
>
Where did you get this definition? I cannot find a definition of
"phenotype" that limits it to *group* characteristics; most sources define
it as either the physical expression of the genotype, or the observable
characteristics of the individual organism, or simply anything you can find
out about the organism without sequencing its genes.
>
> Morphology has to do with individual characteristics, the form and
> structure of individual animals and plants.
>
-- [snip]
>
>>http://w3.fiu.edu/milesk/genetics.htm
>>
>>Let's take a simple case and question: are chihuahuas and St. Bernards
>>99+%
>>similar in morphology (note that not merely size, but proportions and even
>>toe number may vary between these breeds)? Domestic dogs differ from grey
>>wolves by only about 0.2% of their mitochrondrial DNA (and mitochrondrial
>>DNA mutates faster and is more variable than nuclear DNA, which is what we
>>were comparing with humans and chimps above), so the degree of genetic
>>difference between any two dog breeds must be very tiny indeed. I'm not
>>sure how you'd quantify the difference between, e.g. the St. Bernard and
>>the
>>chihuahua, or a greyhound and a dachsund, but I think you'd easily come up
>>with less than 99.9% similarity in appearance, for all that their genetic
>>similarity can be that great.
>
> nuclear DNA produces morphological similarity. MtDNA has to do with
> energy transfer, not morphological similarities. So why are you using
> MtDNA as an example of morphological similarity?
>
I am not; please read more carefully. I am stating that if mtDNA
differences are so tiny, then presumably nuclear DNA differences are even
smaller, so that two dogs can be 99.8% or more genetically identical, and be
as morphologically different as chihuahuas and St. Bernards.
>
-- [snip]
Let me reargue this entire section (i.e. my assertion that major changes in
DNA sequence can have little or no effect on morphology).
The genetic code (the correspondence of three-nucleotide codons to amino
acids that make up proteins) is "degenerate:" rather than having one codon
per amino acid and one for punctuation, most amino acids correspond to
multiple codons (up to six), and there are three separate stop codons. From
this it follows that one could, in principle, make massive changes (ca. 30%
of the sequence) in the genome of any species without making any changes at
all in the proteins produced or the way the organism grows. This are
"silent mutations" -- they have no phenotypic effects at all. Therefore,
logically, one cannot assume that changes in the genome must translate to
changes in the phenotype at all, much less must map one-for-one onto the
changes in the phenotype.
>
>> Or consider this:
>>there is a gene, Pax-6, which triggers eye development in fruit flies.
>>Humans also have a form of Pax-6 (which controls development of the iris
>>of
>>the human eye), which is not identical to the fruit fly version, but
>>experimenters have induced fruit fly eyes to grow on fruit fly wings by
>>introducing *human* Pax-6 genes into the wings (there are, of course,
>>already fruit fly Pax-6 genes in the wings, but they are deactivated).
>>Evidently, fruit flies could develop normally if some of their genes were
>>replaced by their human homologues, which implies, again, that large
>>changes
>>in multiple genes could have little or no noticeable effect.
>
> I don't know how you can draw such a sweeping conclusion from an
> experiment that shows that fruit fly eyes can grow on fruit fly wings.
> Until you present fruit flies that are reproducing successfully with
> eyes on their wings, how can you say that there is no apparent
> difference in function with these changes?
>
The issue is not whether the flies can successfully reproduce (and the
changes to their wings would not be reproduced; these are aquired traits
that do not affect the germ-line DNA). The issue is whether a a PAX-6 gene
that differs from the fruit fly version can do the same job in cells and
tissues that the fruit fly version can. The fact that human PAX-6 triggers
the same effects as fly PAX-6 argues that the fly version of PAX-6 could
mutate to match the human version, without affecting the way fruit flies
develop. They would neither lose their eyes nor start growing
vertebrate-style eyes. Again, a change to genes would *not* map one-to-one
onto a change in morphology.
>
>> The large
>>variations in sequence between cytochrome-c in various species, together
>>with the similarity in function of the enzyme in different species,
>>likewise
>>suggests that changes in genes don't map one-to-one directly to changes in
>>morphology or behavior.
>
> first of all, you need to demonstrate that these variations in
> sequence are really a result of changes over time and not a result of
> original makeup. It's like an ant looking at the differences between
> a car and a plane and saying, "see these differences? They are a
> result of changes that occurred over millions of years." A second ant
> says, "how can you tell this?" The first ant says, "because, can't
> you see that changes occur as a normal course of events? See here,
> rust builds up on this car, and the fender falls off eventually.
> Therefore, given enough time, the car will end up being a plane."
>
First of all, my argument does not depend on the assumption that the
differences between, e.g. human and pine tree cytochrome-c evolved in the
course of descent from a common ancestor. It depends only on the assumption
that human and pine tree cytochrome-c do the same job, engaging in the same
chemical reactions. If this is correct, a mutation or series of mutations
which did change human cytochrome-c to pine tree cytochrome-c would not
alter the way our metabolisms worked or our morphology. That is, not only
can silent mutations produce, in principle, large changes in DNA with no
changes in phenotype, even non-silent mutations could produce very tiny,
inconsequential changes in phenotype. This was one of the points under
contention.
By the way, even if you don't accept (or, I suspect, understand) the
argument about consistent nested hierarchies as evidence for common descent,
at least you could acknowledge that it has been presented to you. The ant
in your little parable offers no argument, not even a bad one, for cars
evolving into aircraft or for the common ancestry of cars and aircraft (of
course, cars and aircraft reproduce rather differently from living things).
>
>>>> It has been known for a long time (since well before the
>>>>discovery of genes) that tiny changes in developmental rates (e.g. how
>>>>long
>>>>a particular structure continues to grow) can produce immense
>>>>differences
>>>>in
>>>>how an organism looks -- and tiny changes in development rates can
>>>>result
>>>>from tiny changes in genes. OTOH, as noted, large sections of many
>>>>proteins
>>>>(and hence the genes that code for them) can be replaced with completely
>>>>different sequences without affecting function.
>>>
>>> references, please?
>>>
>>The classic examples of small changes in genes producing large phenotypic
>>effects are things like four-winged fruit flies (the rear wings are
>>produced
>>by a single mutation modifying the growth of the halteres behind the
>>front -- and in normal flies, only -- wings), or achondroplasty in humans
>>or
>>dogs (a mutation that shortens the limbs).
>
> and these four-winged fruit flies, do they reproduce successfully?
>
Yes. Why should they not? They don't *fly* very successfully, which is the
usual creationist retort at this point, but they reproduce.
>
>>It is well-known that some homologous proteins between different species
>>are
>>very different in sequence (e.g. the aforementioned cytochrome-c, or the
>>even more widely varying fibrins, while others (e.g. the histones that
>>form
>>the backbones of chromosomes) differ very little between species. And
>>I've
>>mentioned that there are variants in hemoglobin within the human species,
>>some of which don't seem to have much in the way of effects. The
>>inference,
>>of course, is that nearly all alterations to histones prevent them from
>>working properly, while hemoglobin and cytochrome-c can vary much more
>>without affecting function.
>>
>>http://alpha2.bmc.uu.se/~lars/biowww/Proteinevol.html
>
> the mistake made here is to assume that differences in sequence arose
> as a result of external mutational change instead of recognizing that
> beneficial differences were there from the beginning.
>
*boggle* That is not right.
*boggle* Apparently bacteria have spent their entire history on Earth
(granted, in your view, that's a much shorter history than in mainstream
science's view) hiding untold myriads of spare beneficial alleles (and a
program for calling them forth) in hyperspace, since neither of these show
up when the bacterial genes are sequenced, but the bacteria keep coming up
with really weird beneficial adaptions (why should a bacterium have the
ability to adapt to eat nylon? is this a problem that's likely to come up in
the natural environment?).
>
> snip>
>
>>> so how do you determine whether an adaptation is inherent or a result
>>> of beneficial mutations? You haven't answered that yet.
>>>
>>You weren't asking that question.
>
> I thought I was.
>
>> With bacteria or fruit flies, watching
>>evolution in real time, one can sequence individuals at the start and end
>>of
>>the experiment and spot the mutations.
>
> and how do you determine that what you are observing are mutations
> from the outside or inherent ability to vary, coming from the inside
> of the genetic system?
>
> It's like watching figures morph in a computer program and claiming
> that the changes are a result of random external mutations when, all
> along, the ability to change was programmed into the morphing figures.
> Have you tracked the source of these changes to determine if they are
> external or internal?
>
Personally, no, though as noted some of these bacterial changes have been
sequenced. And, again, what on earth would lead a reasonable person to
suppose that bacteria had a built-in "ability to adapt" (unless that ability
consisted of the potential to undergo random mutations and natural
selection) for, e.g. the ability to digest poisons not found in nature?
>
-- [snip]
>
>>> as long as you are consistently categorizing the same items, whether
>>> books or cars or life forms, you will always get nested hierarchies
>>> for whatever traits are chosen to be used as a categorizing tool. For
>>> any category chosen, you WILL get the same nested hierarchy because
>>> you are dealing with the same category of things.
>>>
>>But pretty clearly ear bones and mammary glands are not the same things.
>>Having hair and having a single (left) aortic arch (as opposed to having
>>two
>>aortic arches like many reptiles, or a single right arch like birds) are
>>not
>>the same thing either. So why, if you create a category of all
>>vertebrates
>>that have three bones in the inner ear, have you also, automatically,
>>created a category of all vertebrates with mammary glands, a single left
>>aortic arch, and fur?
>
> doesn't mean a thing. Why, if I create a category of all cars that
> have four doors, don't I also automatically create a category of all
> cars with windshields, a steering wheel, and wheels?
>
No. You create a category of cars all of which have all those features, but
there are many cars that have those features and don't have four doors. By
the same token, all animals with three bones in the middle ear and mammary
glands also have vertebrae and pelvic girdles, but not all animals with
vertebrae and pelvic girdles have mammary glands and three bones in the
middle ear.
Note, also, that there's a perfectly good reason all sedans have wheels,
windshields, and a steering wheel (i.e. you don't have much of a car without
these features). One can predict, if I tell you my new car has four doors,
that it has a windshield. You can't predict, on that basis, whether it has
a tape player or CD player, or whether the gear shift lever is on the wheel
or on the console between the seats, because those features vary
independently of the number of doors, because they don't depend on the
number of doors. There's no obvious reason why the utility of mammary
glands is greater for endothermic amniotes with three bones in the middle
ear than for endothermic amniotes with only one bone -- but in point of
fact, only the former have mammary glands.
>
>>If I create a category of all cars with automatic transmissions and four
>>doors, that will not the the same as, or entirely contain, or be entirely
>>contained within, a category of, e.g. "all Ford cars with CD players."
>
> because you have created a category that doesn't fit, is all. If I
> create a category of all vertebrates with three bones in the inner
> ear, it will not be in the same category as vertebrates with wings and
> beaks.
>
But why doesn't the category fit? Why, under "creation theory," did the
Creator not bother to create a single feathered animal with three bones in
the middle ear, or a single mammal with a proper avian-style beak?
>
> It's all subjective.
>
No, but thank you for playing.
>
-- [snip of rest]
>
-- Steven J.
John Harshman
> John Harshman <jharshman....@pacbell.net> writes:
>
>
>>B Richardson wrote:
>>
>>
>>>Ok, I have about 1002 nucleotides for each of Homo Sapiens,
>>>Gorilla Gorilla, Hyloblates Klossii, Pan Troglodytes and Pongo
>>>Pygmaeus from the same gene. If I post the five sets of nucleotides
>>>can you identify which is which based on the patterns of the
>>>similarities you find?
>>
>>I could certainly tell you which was Hylobates and which was Pongo. It's
>>not certain that I could sort out Pan, Homo, and Gorilla, though I would
>>probably be able to make a guess. 1002 nucleotides is not likely to be
>>able to resolve that trichotomy.
>
> Also, even if you had enough nucleotides to get a statistically
> robust resolution of Pan, Homo and Gorilla, you might well still get
> the "wrong" answer. The branching points are close enough that for some
> genes, humans really are more closely related to gorillas than to chimpanzees.
Is it absolutely certain that there has been lineage sorting rather than
homoplasy? We have reason to believe there ought to be lineage sorting,
but I just want to be clear.
Cubist
>B Richardson wrote:
>> Ok, I have about 1002 nucleotides for each of Homo Sapiens,
>> Gorilla Gorilla, Hyloblates Klossii, Pan Troglodytes and Pongo
>> Pygmaeus from the same gene. If I post the five sets of nucleotides
>> can you identify which is which based on the patterns of the
>> similarities you find?
>I could certainly tell you which was Hylobates and which was Pongo. It's
>not certain that I could sort out Pan, Homo, and Gorilla, though I would
>probably be able to make a guess. 1002 nucleotides is not likely to be
>able to resolve that trichotomy.
And, after B. Richardson provided the nucleotide sequences he'd
referred to...
B Richardson wrote:
> John Harshman wrote:
>>OK, here are my identifications:
>>A3 = Hylobates
> Correct.
>>A5 = Pongo
> Correct.
>>A1 = Gorilla
> Correct.
>>A2, A4 = Homo and Pan
> A2 is Homo, A4 is Pan.
This is interesting: Given a description of certain nucleotide data
-- not *the actual data*, but merely *a description of* the data --
Harshman claimed he'd be able to use that data to nail down *exactly*
which one was Hylobates, and which one Pongo; he also claimed that he
might not be able to nail down exactly which ones were Pan, Homo, and
Gorilla, but he could make a guess.
And when he actually *got* the nucleotide data from Richardson...
One: Harshman *did* nail Hylobates and Pongo.
Two: Harshman nailed Gorilla *exactly*
Three: The two sequences for which Harshman's conclusion was "These
two are Pan and Homo, but I can't tell which one is which" actually
*were* Pan and Homo.
"Subjective", eh? To paraphrase Arthur Dent, "This must be some new
meaning of the word 'subjective' with which I was not previously
familiar."
B Richardson
A side note, I had not done a similar analysis on the
dataset before I posted it. The sequences were just a
random find at GenBank.
John Harshman
Like I said: any gene.
Silence from Zoe so far. Do you think she's even reading?
B Richardson
>B Richardson wrote:
>
[snip]
>> No, a taste receptor gene. Take note that the Homo entry says
>> "candidate taste receptor TAS2R38" all the others say
>> "taste receptor type 2 member 38".
>
>The weird thing is that it evolves so fast. They're evolving faster than
>mitochondrial genes in birds. And the transition:transversion bias is
>huge, again comparable to bird mt genes. Is this usual for mammalian
>protein-coding sequences?
>
Dunno, I really don't have any relevant expertise.
These sequences were all 1002 nucleotides in length. What
are the ramifications if the length varies slighty, does
PAUP do the appropriate alignment?
John Harshman
No, you have to provide your own alignment.
Anyway, I think I mentally dropped a zero. In fact, these sequences look
about right for protein-coding. Human-chimp distance is 0.6%, about the
mean for such sequences. And the maximum distance is only 2.5%. The
TI:TV bias still seems big to me, though.
Zoe
<jharshman....@pacbell.net> wrote:
>B Richardson wrote:
snip>
>> Ok, I have about 1002 nucleotides for each of Homo Sapiens,
>> Gorilla Gorilla, Hyloblates Klossii, Pan Troglodytes and Pongo
>> Pygmaeus from the same gene. If I post the five sets of nucleotides
>> can you identify which is which based on the patterns of the
>> similarities you find?
>
>I could certainly tell you which was Hylobates and which was Pongo. It's
>not certain that I could sort out Pan, Homo, and Gorilla, though I would
>probably be able to make a guess. 1002 nucleotides is not likely to be
>able to resolve that trichotomy.
>
>Why are we performing this exercise?
oh, dear, a bigger whoopdedoo is in process.
Have you forgotten my question? It is: Can John establish the
validity of his premise, that similarity has to mean relationship? I
did not ask him if he could identify which species is which, based on
the patterns of similarities found. I asked him to defend his premise
that patterns of similarities must perforce mean common descent and/or
relationship.
There is no challenge on the table for John or anyone else to identify
species by their DNA sequences. I am not questioning John's ability
to figure out which sequences belong to which species, or to even
recognize patterns of similarity and differences. I am asking him to
defend his premise that similarity and/or differences must mean common
descent and/or relationship.
There are too many exceptions that do not mean common descent with
respect to similarity/difference patterns to claim that such patterns
must mean common descent in one particular area.
B Richardson
>
>B Richardson wrote:
>
>> John Harshman wrote:
>>
>>>B Richardson wrote:
>>>
>>
>>
>> [snip]
>>
>>
>>>>No, a taste receptor gene. Take note that the Homo entry says
>>>>"candidate taste receptor TAS2R38" all the others say
>>>>"taste receptor type 2 member 38".
>>>
>>>The weird thing is that it evolves so fast. They're evolving faster than
>>>mitochondrial genes in birds. And the transition:transversion bias is
>>>huge, again comparable to bird mt genes. Is this usual for mammalian
>>>protein-coding sequences?
>>>
>>
>>
>> Dunno, I really don't have any relevant expertise.
>>
>> These sequences were all 1002 nucleotides in length. What
>> are the ramifications if the length varies slighty, does
>> PAUP do the appropriate alignment?
>
>No, you have to provide your own alignment.
>
Do you have the tools at your disposal to do this? Say
if most of the sequences were around 1740 in length
and typically varied by 4 or 5 and if there was a single
outlier at around 1500 in length, Is this workable?
>
>Anyway, I think I mentally dropped a zero. In fact, these sequences look
>about right for protein-coding. Human-chimp distance is 0.6%, about the
>mean for such sequences. And the maximum distance is only 2.5%. The
>TI:TV bias still seems big to me, though.
>
>
Commenting on the TI:TV bias is beyond my knowledge base, if
you weren't Harshman I would say "ask Harshman".
B Richardson
Hard to say. I vaguely remember that she has left threads for
up to a few days at a time and then later revisit them. Hard
to say if she is thinking things over when she does that or
getting distracted by daily life. One can only hope that she
has read or will read the excercise and pose some well thought
out questions/comments.
shane
Seconded
--
shane
And the truth shall set you free.
B Richardson
The same thing could be done to identify various members
of the human population where relation is documented by
historical record using the *same* algorithm on the
polymorphisms, the technique doesn't even work if there
is no relation. Knowing how descent works is the only means
that Harshman had at his disposal to identify the various
members. If you have a competing explanation that can produce
answers bring it to the table, at least table some of the
exceptions you allude to for discussion.
John Harshman
> John Harshman wrote:
>
>>B Richardson wrote:
>>
>>
>>>John Harshman wrote:
>>>
>>>
>>>>B Richardson wrote:
>>>>
>>>
>>>
>>>[snip]
>>>
>>>
>>>
>>>>>No, a taste receptor gene. Take note that the Homo entry says
>>>>>"candidate taste receptor TAS2R38" all the others say
>>>>>"taste receptor type 2 member 38".
>>>>
>>>>The weird thing is that it evolves so fast. They're evolving faster than
>>>>mitochondrial genes in birds. And the transition:transversion bias is
>>>>huge, again comparable to bird mt genes. Is this usual for mammalian
>>>>protein-coding sequences?
>>>>
>>>
>>>
>>>Dunno, I really don't have any relevant expertise.
>>>
>>>These sequences were all 1002 nucleotides in length. What
>>>are the ramifications if the length varies slighty, does
>>>PAUP do the appropriate alignment?
>>
>>No, you have to provide your own alignment.
>
> Do you have the tools at your disposal to do this? Say
> if most of the sequences were around 1740 in length
> and typically varied by 4 or 5 and if there was a single
> outlier at around 1500 in length, Is this workable?
There are many programs that will do alignments for you, of which
Clustal is the most popular. I find that Eyeball Mark I is superior to
all of them. I use MacClade, which displays a multiple alignment in
convenient format, and lets you move blocks of sequence around easily.
>>Anyway, I think I mentally dropped a zero. In fact, these sequences look
>>about right for protein-coding. Human-chimp distance is 0.6%, about the
>>mean for such sequences. And the maximum distance is only 2.5%. The
>>TI:TV bias still seems big to me, though.
>
> Commenting on the TI:TV bias is beyond my knowledge base, if
> you weren't Harshman I would say "ask Harshman".
Will anyone who knows mammal nuclear coding sequences comment on this?
Anyone? Anyone?
John Harshman
> On Thu, 04 Aug 2005 17:04:01 GMT, John Harshman
> <jharshman....@pacbell.net> wrote:
>
>
>>B Richardson wrote:
>
>
> snip>
>
>>>Ok, I have about 1002 nucleotides for each of Homo Sapiens,
>>>Gorilla Gorilla, Hyloblates Klossii, Pan Troglodytes and Pongo
>>>Pygmaeus from the same gene. If I post the five sets of nucleotides
>>>can you identify which is which based on the patterns of the
>>>similarities you find?
>>
>>I could certainly tell you which was Hylobates and which was Pongo. It's
>>not certain that I could sort out Pan, Homo, and Gorilla, though I would
>>probably be able to make a guess. 1002 nucleotides is not likely to be
>>able to resolve that trichotomy.
>>
>>Why are we performing this exercise?
>
>
> oh, dear, a bigger whoopdedoo is in process.
>
> Have you forgotten my question? It is: Can John establish the
> validity of his premise, that similarity has to mean relationship? I
> did not ask him if he could identify which species is which, based on
> the patterns of similarities found. I asked him to defend his premise
> that patterns of similarities must perforce mean common descent and/or
> relationship.
How would one do this, other than the way I have done it already?
The way I've done it is to establish that a nested hierarchy exists, and
is recoverable from any genetic data you would care to present (which is
the point of this exercise). I advance common descent as an explanation
for this hierarchy. What other explanation do you have that's tenable?
If you can't think of one, we must provisionally accept common descent.
That's all science ever does, though there are certainly degrees of
"provisional". At the moment, common descent of apes is about as
non-provisional as you can get.
> There is no challenge on the table for John or anyone else to identify
> species by their DNA sequences. I am not questioning John's ability
> to figure out which sequences belong to which species, or to even
> recognize patterns of similarity and differences. I am asking him to
> defend his premise that similarity and/or differences must mean common
> descent and/or relationship.
>
> There are too many exceptions that do not mean common descent with
> respect to similarity/difference patterns to claim that such patterns
> must mean common descent in one particular area.
What particular exceptions are you talking about here?
Eric Rowley
> >B Richardson wrote:
> snip>
>>> Ok, I have about 1002 nucleotides for each of Homo Sapiens,
>>> Gorilla Gorilla, Hyloblates Klossii, Pan Troglodytes and
>>> Pongo Pygmaeus from the same gene. If I post the five sets of
>>> nucleotides can you identify which is which based on the
>>> patterns of the similarities you find?
> > I could certainly tell you which was Hylobates and which was
> > Pongo. It's >not certain that I could sort out Pan, Homo, and
> > Gorilla, though I would >probably be able to make a guess.
> > 1002 nucleotides is not likely to be able to resolve that
> > trichotomy.
> >Why are we performing this exercise?
> oh, dear, a bigger whoopdedoo is in process.
> Have you forgotten my question? It is: Can John establish the
> validity of his premise, that similarity has to mean
> relationship? I did not ask him if he could identify which
> species is which, based on the patterns of similarities found.
You have previously asserted that the nested hierarchy is
arbitrary, based on subjective decisions, formed by putting
a species where it is thought to belong acording to the
evolutionist world view (or am I confusing you with someone else?)
John has just clearly demonstrated that this is not the case,
by placing the species in their correct places without knowing
which was which.
> I asked him to defend his premise that patterns of similarities
> must perforce mean common descent and/or relationship.
What else could they mean?
There is no other explanation for the existance of the nested
hierarchy.
> There is no challenge on the table for John or anyone else to
> identify species by their DNA sequences. I am not questioning
> John's ability to figure out which sequences belong to which
> species, or to even recognize patterns of similarity and
> differences.
Consider it a challange to _you_ to explain how he was able to
do it, if the nested hierarchy is arbitrary as you claim there
should be no way to get it "right" without knowing which sequence
belonged to which species.
> I am asking him to defend his premise that
> similarity and/or differences must mean common
> descent and/or relationship.
> There are too many exceptions that do not mean common descent
> with respect to similarity/difference patterns
No there aren't.
A complex and consistant nested hierarchy based on all of the
properties of the studied items is a very good identifier of
common descent with modification.
There is no other mechanism known that produces them.
All of your attempts to force things into a nested hierarchy
have involved ignoring most or all (in the case of the sweaters)
of their actual properties and defining them into arbitrary
categories.
> to claim that
> such patterns must mean common descent in one particular area.
They always do, in all areas.
(If they are unforced and based on the actual properties of
the items.
Eric
B Richardson
The reason I asked is I've collected another gene for each of
Pan troglodytes
Gorilla gorilla
Pongo pygmaeus
Hylobates lar
Macaca fascicularis
Macaca nemestrina
Colobus guereza
Ateles geoffroyi
There is a slight variation in the lengths, a single outlier is about
200 nucleotides shorter than the others.
-
#include "signature"
John Harshman
In my experience, that should be quite easy to do by eye. I would
suggest aligning the roughly equal sequences to each other before
aligning the short one to the rest. You do this by inserting - into
sequences until they match each other.
B Richardson
>B Richardson wrote:
>
[snip]
>>
>>
>> ...I've collected another gene for each of
>>
>> Pan troglodytes
>> Gorilla gorilla
>> Pongo pygmaeus
>> Hylobates lar
>> Macaca fascicularis
>> Macaca nemestrina
>> Colobus guereza
>> Ateles geoffroyi
>>
>> There is a slight variation in the lengths, a single outlier is
about
>> 200 nucleotides shorter than the others.
>
>In my experience, that should be quite easy to do by eye. I would
>suggest aligning the roughly equal sequences to each other before
>aligning the short one to the rest. You do this by inserting -
into
>sequences until they match each other.
>
>
[snip]
Weedhopper has come back.
I've aligned them with an online tool (ClustalW) and
loaded into PHYLIP. Below is the tree, the neighbor
joining tree was the same save from slight differences
in branch lengths. Simply multiplying the length by 1000
gave a scale that fits on an 80 column screen well (except
for B4) and I've scaled the branch lengths accordingly.
Looking at the tree, I see two pairs that the best you
can lock it down to is either/or, and the reason seems
obvious. I guessed that the one that was more than
150 nucleotides that the rest would be the longest
branch and let it be the outgroup.
Any takers?
DNA parsimony algorithm, version 3.64
One most parsimonious tree found:
<pre>
+----------------------B8
+------------------6
| | +---------------B7
| +--------5
| +-------------B6
|
3--------------[off the page]------------------------------B4
|
| +----------------------B5
+---------------4
| +----------------B2
+-----1
| +---------B3
+----------2
+-----------B1
</pre>
requires a total of 724.000
between and length
------- --- ------
3 6 0.019183
6 B8 0.021795
6 5 0.009497
5 B7 0.015052
5 B6 0.013058
3 B4 0.241548
3 4 0.015954
4 B5 0.022412
4 1 0.006173
1 B2 0.016239
1 2 0.011111
2 B3 0.009117
2 B1 0.011396
John Harshman
Why not?:
> +----------------------B8 Colobus
> +------------------6
> | | +---------------B7
> | +--------5 } Macaca
> | +-------------B6
> |
> 3--------------[off the page]------------------------------B4 Ateles
> |
> | +----------------------B5 Hylobates
> +---------------4
> | +----------------B2 Pongo
> +-----1
> | +---------B3
> +----------2 }Gorilla, Pan
> +-----------B1
But surely there's a Homo sequence. You can find it easily on genbank by
BLASTING the Pan sequence. Or go to the UCSC genome browser and BLAT it.
Ernest Major
<br...@nym.hush.com> writes
The shorter sequence might be because the sequence is incomplete, rather
than because the gene actually is shorter (there's one gene and clade
I've looked at where about one third of the published sequences are the
first half of the gene, one third the second half of the gene, and one
third the whole gene). Depending on exactly what you told PHYLIP
(missing data or absent base pair) this may have thrown the result off.
With that proviso, you have one cluster of 4 hominoids, one cluster of 3
cercopithecoids, and one ceboid, i.e.
B1/B3 Pan troglodytes/Gorilla gorilla
B2 Pongo pygmaeus
B4 Ateles geoffroyi
B5 Hylobates lar
B6/B7 Macaca fascicularis/nemestrina
B8 Colobus guereza
You may have been wiser to eliminate the parts of the other sequences
corresponding to the missing bases.
--
alias Ernest Major
--
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Checked by AVG Anti-Virus.
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B Richardson
The shorter sequence was brought up to length by infilling with
some '-'s, I'll have to pour thru the docs to find out what
treatment it gave those.
>
>With that proviso, you have one cluster of 4 hominoids, one cluster of 3
>cercopithecoids, and one ceboid, i.e.
>
>B1/B3 Pan troglodytes/Gorilla gorilla
>B2 Pongo pygmaeus
>B4 Ateles geoffroyi
>B5 Hylobates lar
>B6/B7 Macaca fascicularis/nemestrina
>B8 Colobus guereza
>
Correct on all counts.
>
>You may have been wiser to eliminate the parts of the other sequences
>corresponding to the missing bases.
>
Wouldn't that effectively just produce a better branch length for
Ateles only, and slightly reduce the amount of information available
to sort out all the others?
B Richardson
Correct on all counts.
>
>But surely there's a Homo sequence. You can find it easily on genbank by
>BLASTING the Pan sequence. Or go to the UCSC genome browser and BLAT it.
>
>
I just found it, I didn't think to look at the website earlier.
The others I've been plucking out of a big file I downloaded
from their ftp site a while back and it didn't have the Homo
sequence. They have more nucleotides for the Homo sequence.
The gene is semenogelin II
Homo sapiens
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=Nucleotide&dopt=GenBank&val=M81652
http://tinyurl.com/b7hxf
Pan troglodytes
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=55419662
http://tinyurl.com/bd2cc
Gorilla gorilla
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=55419664
http://tinyurl.com/8fdrj
Pongo pygmaeus
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=55419666
http://tinyurl.com/abdvh
Hylobates lar
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=55419668
http://tinyurl.com/dh9ay
Macaca fascicularis
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=55419670
http://tinyurl.com/7csap
Macaca nemestrina
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=55419672
http://tinyurl.com/7nqdd
Colobus guereza
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=55419674
http://tinyurl.com/a5yao
Ateles geoffroyi
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=55419676
http://tinyurl.com/7wf8k
Ernest Major
know that in advance. If you had replaced a large chunk of one of the
Macaca sequences with '-'s it might have broken the cladogram - IIRC, '
' is no data, and '-' is a "deletion" - depending on how PHYLIP handles
deletions it might have made the modified sequence appear far removed. I
suspect that the code treats indels as single events, but I don't know
this to be the case, and the length of the branch to Ateles suggests
otherwise.
(I'm afraid I'm guilty of 'plug and chug' with PHYLIP.)
John Harshman
The default is missing data, so I wouldn't worry.
> With that proviso, you have one cluster of 4 hominoids, one cluster of 3
> cercopithecoids, and one ceboid, i.e.
>
> B1/B3 Pan troglodytes/Gorilla gorilla
> B2 Pongo pygmaeus
> B4 Ateles geoffroyi
> B5 Hylobates lar
> B6/B7 Macaca fascicularis/nemestrina
> B8 Colobus guereza
>
> You may have been wiser to eliminate the parts of the other sequences
> corresponding to the missing bases.
Bad practice. Lowers resolution. Deleting data is seldom a good idea.
John Harshman
Phylip treats - as missing data. No problem. Well, it can cause some
problems with neighbor joining if the missing section differs
substantially in evolutionary rate from the rest of the gene. But he
used parsimony anyway, I do believe.
Zoe
<sjt195...@nts.link.net.INVALID> wrote:
snip>
>> Steven, I'm talking about the usefulness of probability and statistics
>> in explaining how a cardboard box is put together or in determining
>> how chromosomes are consistently the same for any group of life forms.
>> It isn't useful for these purposes, is it?
>>
>Well, no. But before you were talking about the usefulness of probability
>in constructing cardboard boxes, you were talking about random mutations as
>though the laws of probability did not apply to them.
I trust your summarization of what went before, so will snip it.
If you say that I said that the laws of probability did not apply to
random mutations, then I take that back. I did not mean that. I agree
that probability and statistics can make a reasonable estimate as to
the chance of a certain random event happening, IF it gets the
background data right. It can predict the chances of fusion happening
if it knows that several populations have 24-chromosome members, or of
fission happening if a single population has 23-chromosome members.
But it seems to me that probability and statistics will be only as
good as its source information.
What is the source information for chromosome fission or fusion?
Apparently, the basis on which you decide that the last common
ancestor was more likely to have 24 chromosomes is because all apes
except humans have 24 chromosomes. You conclude that there is more of
a chance for fusion rather fission because there are (present tense)
more populations of 24's available for the random fusing mutation, and
less of a chance for the random fissioning mutation to hit a single
population of 23's. But the probability is calculated on what exists
today and not on the original population, which is what I think should
be used.
Besides that, I submit that, as an evolutionist, there is no reason to
reject or accept either scenario since, in principle, evolutionary
theory starts with a lesser number and evolves into greater numbers,
anyway. As well as, there is no predictability. Take, for instance,
a LCA that has 23 chromosomes. It may be probable that a chance
mutation can come along that causes fission in a chromosome, and a new
population eventually emerges (according to your theory) where its
members carry 24 chromosomes. And since mutations are random, meaning
that all possible mutations have equal probability of selection, then
humans (according to your theory) could have descended from the
original population that had 23 chromosomes, and the population with
the new 24th chromosome, through geographical isolation (according to
your theory) could be hit with other mutations (according to your
theory) that would cause the first 24-chromosome population to
continue to vary into your gorillas and other ape types (according to
your theory).
So, having sat inside of your evolutionary box for the last few
minutes, I don't see how you could use probability and statistics to
conclude that fusion is the more likely event when you don't know the
background of your proposed populations. You are assuming, without
grounds, that the LCA had 24 chromosomes, not 23. And this assumption
is based on the supposedly evolved populations of apes existing today,
instead of on the theorized first split in a population that could
have carried either 23 chromosomes or 24 chromosomes.
I think that probability and statistics is valid for known situations,
but not for the unknown. It has to be known that someone is
consistently, non-randomly flipping a coin thousands of times, and
only then can that background information be used in a probability and
statistics prediction of the chances of getting heads or tails. But
if someone is not consistently flipping a coin, but just randomly,
non-repetitively tossing a coin, a toss today, two tosses tomorrow, no
tosses for a week, a series of tosses in a single hour, and so on, is
there a way for probability and statistics to predict random behavior
that is based on random behavior?
I hope some statistician will clear that up for me, because right now
it doesn't make sense. I see the chances of a LCA having 23
chromosomes versus 24 as a totally random happening (according to your
theory). The random mutation could be hitting either a 23-chromosome
population or a 24-chromosome population, and there's no way to know
which. How does P&S predict realistically if the background
information is unknown?
And that is why, when it is claimed that random mutations can produce
the complexity seen in nature, and that, based on probability and
statistics, sooner or later you're going to get that lucky strike, I
tend to think to myself, What? NO WAY. Why no way? Because the
background information is such that it is impossible for P&S to work.
It is one thing to say that the probability of winning the lottery of
$20 million is X, but that is because the background data is a
reality. There is a pot of $20 million waiting to be won.
Eventually, sooner or later, someone will hit that jackpot. With
evolutionary theory, there is no pot of gold waiting to be won. There
is no concrete data in the pot. And you can't predict on what you
don't know. There is no chance of winning something out of nothing.
Okay, so detour's over. May I now revert to the original intent of my
threads, which is to establish how mental activity is recognized? And
I believe the last thing I requested was for an explanation of how,
absent mental activity, random mutations are expected to achieve the
formation of a digestive system, going from a single cell (which is an
overly generous "given") to a system within systems that includes the
digestive system.
>>>> So now, are you saying that random events are credited with pulling
>>>> together a digestive system or a circulatory system or a cardboard
>>>> box? Or are you taking a fully-formed reproductive system and
>>>> applying your evolutionary theory of mutations to it? I am really
>>>> interested in the construction of the system, not in the mutations
>>>> that can happen to the construction.
>>>>
>>>No, I am not saying that random events are credited with putting together
>>>a
>>>digestive system (at least, not by themselves); random events in
>>>combination
>>>with natural selection (reproduction, variation, and differential
>>>reproductive success) put complex structures together.
>>
>> and this is the process that has not yet been explained by posters to
>> TO -- not one. Please describe a scenario, based on facts, not
>> fantasy, of how a digestive system comes together through random
>> events in combination with natural selection. And you cannot use
>> reproduction, variation, and differential reproductive success unless
>> you are willing to concede that the machinery was already in place,
>> fully functioning, after which comes along your mutations and
>> selection.
>>
>I suspect you're asking me for a mutation by mutation, selective regime by
>selective regime, account of how the human digestive tract evolved from a
>single-celled organism. I cannot, of course, provide any such thing.
and why not? Based on your scientific, observed data of how mutations
behave, surely you can plug that data into your evolutionary scenario
and scientific observations of how mutations and selection work in
describing a realistic step-by-step pathway on how a digestive system
can come into existence. If you can't do this, then I must take your
declaration on faith...which I am not inclined to do.
> I
>also suspect that you have neither the intention nor the ability to tell us
>how "intelligence" (other, perhaps, than human intelligence) implements any
>"design" or change in design in living organisms.
I cannot make a digestive system, so I cannot tell you how to do it.
But if I were to try to recreate something that works like the
digestive system, I certainly would not try to do it by random
mutations. Would you? I would take note of the steps taken in a
what-you-see-is-what-you-get system, and attempt to copy those, as far
as possible. And that would be a useful, scientific venture, learning
from nature, copying its processes, rather than speculating on its
history.
>> So, okay, we have a simple common ancestor consisting of a single
>> functioning cell (and even that is a generous given) that replicates
>> (we know not how that started). Take it from there and describe a
>> realistic scenario, using factual, scientific observations, as to how
>> this single cell develops a digestive system, based on random
>> mutations and selection.
>>
>> Can't do it? Then evolutionists need to be a little humbler about
>> their position. To say "We know the digestive system evolved," but go
>> silent when the question of "how?" is asked, is to ask thinking minds
>> to take your word on faith.
>>
>Don't be silly, Zoe. It is perfectly possible to demonstrate that something
>happened, without having a complete description of how it happened. Your
>position is tantamount to saying that if we can't figure out how someone
>died, we are not justified in inferring that he is dead.
the issue is not about whether someone is dead or whether something
happened. It is about HOW something happened. My position is
tantamount to saying that if we can't figure out how someone died, we
are not justified in making up stories about how he died. There is no
controversy over whether the person is dead. Neither is there
controversy that we exist.
>You have, in the consistent nested hierarchy of homologies,
you have yet to demonstrate that nested hierarchies always mean common
descent. If they do not always mean common descent, then on what
basis do you decide that only the nested hierarchies of nature mean
common descent?
> in biogeography,
why does biogeography mean common descent, unless there is a
preconceived notion in place?
>in vestigial structures at the genetic and morphological level,
the term "vestigial structures" is a term arising out of preconceived
notions. Some may call the appendix vestigial, but there are uses for
the appendix. Some may call the tailbone vestigial, but there are
uses for the tailbone...and so on. To call something vestigial
because it seems to have no use is a misunderstanding of and
egotistical dismissal of structures that are really not vestigial at
all.
> in the
>fossil record,
the fossil record is subject to interpretation.
>in the jury-rigged and improvised nature of many adaptions
>(e.g. Darwin's remark on "similar structures for dissimilar functions and
>dissimilar structures for similar functions"), compelling evidence for
>common descent with modification.
nothing compelling so far to this creationist.
>You have, furthermore, an demonstrated mechanism of mutation and natural
>selection.
this is a mechanism that fails to produce a digestive system, so how
has it been demonstrated? Instead, you want your systems to be fully
in place and operating a la creation, and then you begin to apply your
theory of random mutations to these ready-made systems. You can't
have this head start unless you acknowledge that the system was in
place, fully functioning, from the beginning -- which is the position
of creation theory.
> It has produced, in the lab, bacteria resistant to poisons never
>found in nature,
the ability to respond to changes in the environment, including
poisons never found in nature, is an inherent ability.
> bacteria that *eat* poisons never found in nature,
as long as the bacterium is programmed to respond to alien influences,
including poisons never found in nature, it will adapt to these alien
influences, or die, depending on its health.
>multicellular colonial organisms evolved from single-celled ancestors,
I submit you are observing a programmed ability to divde, and are
mistakenly calling it evolution.
> and
>similar examples of striking novel traits. It seems to me that you are not
>being asked to accept anything on "faith," but on the basis of considerable
>evidence regarding both the fact and the proposed mechanism for it.
faith is called upon to rely on your interpretation of the above data,
Steven.
>> So, here we go.
>>
>> A single cell exists, replicating itself repeatedly. Along comes a
>> random "beneficial mutation." What happens next, based on your
>> selection principle? How does the digestive system develop?
>>
>It becomes a multicellular organism.
could you be a little less vague? So you think that a single cell
becoming multicellular is how a digestive system forms? Have you
accounted for the changes in DNA sequences that are needed to produce
the particular types of proteins needed to construct an esophagus, a
stomach, duodenum, jejunum, small intestines, and all the attendant
parts that make a digestive system work?
> http://www.gate.net/~rwms/EvoMutations.html
>
>Starting from single celled animals, each of which has the capability to
>reproduce there is no sex in the sense that we think of the term. Selective
>pressure has been observed to convert single-cellular forms into
>multicellular forms. A case was observed in which a single celled form
>changed to multicellularity.
>Boxhorn, a student of Boraas,writes:
>Coloniality in Chlorella vulgaris
>Boraas (1983) reported the induction of multicellularity in a strain of
>Chlorella pyrenoidosa (since reclassified as C. vulgaris) by predation. He
>was growing the unicellular green alga in the first stage of a two stage
>continuous culture system as for food for a flagellate predator, Ochromonas
>sp., that was growing in the second stage. Due to the failure of a pump,
>flagellates washed back into the first stage. Within five days a colonial
>form of the Chlorella appeared. It rapidly came to dominate the culture. The
>colony size ranged from 4 cells to 32 cells. Eventually it stabilized at 8
>cells. This colonial form has persisted in culture for about a decade. The
>new form has been keyed out using a number of algal taxonomic keys. They key
>out now as being in the genus Coelosphaerium, which is in a different family
>from Chlorella. "
>
>Boraas, M. E. 1983. Predator induced evolution in chemostat culture. EOS.
>Transactions of the American Geophysical Union. 64:1102.
okay, so far you've gotten your single cell to become multicellular.
Is this the digestive system?
>There are, of course, an immense number of steps along the way: the
>development of multiple layers (starting with something cnidarian-like with
>two layers of cells, and gradually evolving (in some lineages) a third
>layer), the innermost of which may be devoted to digesting food (note that
>the single cell, and its simple colonial descendants, already can take in
>food through their surface, so what we are talking about here is having some
>fraction of the body cells specialize in a function they already have).
and how do you propose selected random mutations achieve the
conversion of some cells into specialized functions? If you have no
pathway, then merely saying "it evolved" is asking thinking minds to
take your word by faith.
>-- [snip]
>>
>>>What is your definition of "phenotype," and how does "phenotype" differ
>>>from
>>>"morphology?"
>>
>> phenotype has to do with group characteristics, psychological and
>> anatomical, resulting from both heredity and environment. It refers
>> to characteristics of organisms collectively, or a group of organisms
>> having like characteristics.
>>
>Where did you get this definition? I cannot find a definition of
>"phenotype" that limits it to *group* characteristics; most sources define
>it as either the physical expression of the genotype, or the observable
>characteristics of the individual organism, or simply anything you can find
>out about the organism without sequencing its genes.
I got my definition from a standard dictionary.
>> Morphology has to do with individual characteristics, the form and
>> structure of individual animals and plants.
>>
>-- [snip]
>>
>>>http://w3.fiu.edu/milesk/genetics.htm
>>>
>>>Let's take a simple case and question: are chihuahuas and St. Bernards
>>>99+%
>>>similar in morphology (note that not merely size, but proportions and even
>>>toe number may vary between these breeds)? Domestic dogs differ from grey
>>>wolves by only about 0.2% of their mitochrondrial DNA (and mitochrondrial
>>>DNA mutates faster and is more variable than nuclear DNA, which is what we
>>>were comparing with humans and chimps above), so the degree of genetic
>>>difference between any two dog breeds must be very tiny indeed. I'm not
>>>sure how you'd quantify the difference between, e.g. the St. Bernard and
>>>the
>>>chihuahua, or a greyhound and a dachsund, but I think you'd easily come up
>>>with less than 99.9% similarity in appearance, for all that their genetic
>>>similarity can be that great.
>>
>> nuclear DNA produces morphological similarity. MtDNA has to do with
>> energy transfer, not morphological similarities. So why are you using
>> MtDNA as an example of morphological similarity?
>>
>I am not; please read more carefully. I am stating that if mtDNA
>differences are so tiny, then presumably nuclear DNA differences are even
>smaller, so that two dogs can be 99.8% or more genetically identical, and be
>as morphologically different as chihuahuas and St. Bernards.
this is an assumption without foundation. Just because mtDNA
differences are tiny, there is no reason to presume (your word),
without evidence, that nuclear DNA differences are even smaller.
Indeed, as mentioned earlier, after chimp/human genome comparison, it
has been noted that the differences are 83%, so definitely not
smaller.
>-- [snip]
>
>Let me reargue this entire section (i.e. my assertion that major changes in
>DNA sequence can have little or no effect on morphology).
>
>The genetic code (the correspondence of three-nucleotide codons to amino
>acids that make up proteins) is "degenerate:" rather than having one codon
>per amino acid and one for punctuation, most amino acids correspond to
>multiple codons (up to six), and there are three separate stop codons. From
>this it follows that one could, in principle, make massive changes (ca. 30%
>of the sequence) in the genome of any species without making any changes at
>all in the proteins produced or the way the organism grows.
I'm not sure what you mean by "massive" here. That these codons allow
for the morphing of a species into another? What exactly are these
massive changes?
> This are
>"silent mutations" -- they have no phenotypic effects at all. Therefore,
>logically, one cannot assume that changes in the genome must translate to
>changes in the phenotype at all, much less must map one-for-one onto the
>changes in the phenotype.
these variations of codons for protein don't vary the proteins to the
point where you have change in morphology, so why use them as evidence
at all then?
>>> Or consider this:
>>>there is a gene, Pax-6, which triggers eye development in fruit flies.
>>>Humans also have a form of Pax-6 (which controls development of the iris
>>>of
>>>the human eye), which is not identical to the fruit fly version, but
>>>experimenters have induced fruit fly eyes to grow on fruit fly wings by
>>>introducing *human* Pax-6 genes into the wings (there are, of course,
>>>already fruit fly Pax-6 genes in the wings, but they are deactivated).
>>>Evidently, fruit flies could develop normally if some of their genes were
>>>replaced by their human homologues, which implies, again, that large
>>>changes
>>>in multiple genes could have little or no noticeable effect.
>>
>> I don't know how you can draw such a sweeping conclusion from an
>> experiment that shows that fruit fly eyes can grow on fruit fly wings.
>> Until you present fruit flies that are reproducing successfully with
>> eyes on their wings, how can you say that there is no apparent
>> difference in function with these changes?
>>
>The issue is not whether the flies can successfully reproduce
it most certainly is the issue. You are asserting that changes such
as seen done in the fruit fly are evidence for evolution of the
species. If the flies cannot successfully reproduce, then you don't
have a species that can continue to morph. End of the line. No
macroevolution along that fruit-fly line.
> (and the
>changes to their wings would not be reproduced; these are aquired traits
>that do not affect the germ-line DNA).
worse yet. Then that's the end of that genetic change for sure.
> The issue is whether a a PAX-6 gene
>that differs from the fruit fly version can do the same job in cells and
>tissues that the fruit fly version can. The fact that human PAX-6 triggers
>the same effects as fly PAX-6 argues that the fly version of PAX-6 could
>mutate to match the human version, without affecting the way fruit flies
>develop.
can't happen, not if the species with this gene cannot reproduce.
Indeed, if it is an acquired trait, as you state above, then it's
certainly not going to be passed down to eventually form a new
species, even if the fly could still reproduce.
>They would neither lose their eyes nor start growing
>vertebrate-style eyes. Again, a change to genes would *not* map one-to-one
>onto a change in morphology.
but neither would the changes carry on into future generations. What
good is this to the evolution of a new species? Your whole point is
becoming more and more moot.
>>> The large
>>>variations in sequence between cytochrome-c in various species, together
>>>with the similarity in function of the enzyme in different species,
>>>likewise
>>>suggests that changes in genes don't map one-to-one directly to changes in
>>>morphology or behavior.
>>
>> first of all, you need to demonstrate that these variations in
>> sequence are really a result of changes over time and not a result of
>> original makeup. It's like an ant looking at the differences between
>> a car and a plane and saying, "see these differences? They are a
>> result of changes that occurred over millions of years." A second ant
>> says, "how can you tell this?" The first ant says, "because, can't
>> you see that changes occur as a normal course of events? See here,
>> rust builds up on this car, and the fender falls off eventually.
>> Therefore, given enough time, the car will end up being a plane."
>>
>First of all, my argument does not depend on the assumption that the
>differences between, e.g. human and pine tree cytochrome-c evolved in the
>course of descent from a common ancestor. It depends only on the assumption
>that human and pine tree cytochrome-c do the same job, engaging in the same
>chemical reactions.
it makes sense, based on the behavior of creative mental activity,
that a particular gene would be used in the master plan for all life
forms, but switched on for some life forms and switched off for other
life forms. When switched off, it is not even recognizable as a gene,
but is just part of the material that is presently called junk. Why
switch this gene off? I might want to give certain life forms the
ability to enjoy citrus fruit and therefore switch off that gene so
that there is not an overload of vitamin C?
> If this is correct, a mutation or series of mutations
>which did change human cytochrome-c to pine tree cytochrome-c would not
>alter the way our metabolisms worked or our morphology. That is, not only
>can silent mutations produce, in principle, large changes in DNA with no
>changes in phenotype, even non-silent mutations could produce very tiny,
>inconsequential changes in phenotype. This was one of the points under
>contention.
meaning you can have it working for you all ways, coming and going --
sounds very much like a sweeping "mutationsdidit" with no further
explanation.
>
>By the way, even if you don't accept (or, I suspect, understand) the
>argument about consistent nested hierarchies as evidence for common descent,
>at least you could acknowledge that it has been presented to you. The ant
>in your little parable offers no argument, not even a bad one, for cars
>evolving into aircraft or for the common ancestry of cars and aircraft (of
>course, cars and aircraft reproduce rather differently from living things).
the ant is an apt example of human thinking in relation to the things
we don't understand. The ant might think, if it could think, that it
has a great argument for how a car changes into an airplane. It is an
ant's perspective. Relatively speaking, humans are like ants.
snip>
>>>The classic examples of small changes in genes producing large phenotypic
>>>effects are things like four-winged fruit flies (the rear wings are
>>>produced
>>>by a single mutation modifying the growth of the halteres behind the
>>>front -- and in normal flies, only -- wings), or achondroplasty in humans
>>>or
>>>dogs (a mutation that shortens the limbs).
>>
>> and these four-winged fruit flies, do they reproduce successfully?
>>
>Yes. Why should they not? They don't *fly* very successfully, which is the
>usual creationist retort at this point, but they reproduce.
is there a growing population of four-winged fruit flies in existence
somewhere? What are they called? Are they out and surviving in the
wild or cultured only in a lab?
>>>It is well-known that some homologous proteins between different species
>>>are
>>>very different in sequence (e.g. the aforementioned cytochrome-c, or the
>>>even more widely varying fibrins, while others (e.g. the histones that
>>>form
>>>the backbones of chromosomes) differ very little between species. And
>>>I've
>>>mentioned that there are variants in hemoglobin within the human species,
>>>some of which don't seem to have much in the way of effects. The
>>>inference,
>>>of course, is that nearly all alterations to histones prevent them from
>>>working properly, while hemoglobin and cytochrome-c can vary much more
>>>without affecting function.
>>>
>>>http://alpha2.bmc.uu.se/~lars/biowww/Proteinevol.html
>>
>> the mistake made here is to assume that differences in sequence arose
>> as a result of external mutational change instead of recognizing that
>> beneficial differences were there from the beginning.
>>
>*boggle* That is not right.
that's all you got to say, Steven? That's not right? Okay, then I
will respond that it is, too, right. :-\
snip>
>>>http://www.talkorigins.org/faqs/mutations.html#Q2 has a list of favorable
>>>mutations in various species, which would certainly seem to answer your
>>>request.
>>
>> please, not the same old tired list of six examples. In any event,
>> what you call favorable mutations, I call inherent ability to vary or
>> adapt to environmental stimuli. How are we going to demonstrate which
>> is correct? I'm betting there is no predictability test or
>> explanatory test that will demonstrate that these responses to the
>> environment are really favorable mutations from the outside. However,
>> creation theory would predict that favorable adjustments to
>> environmental stimuli (what you call favorable mutations) can be
>> traced to an internal program that allows for such variations.
>>
>*boggle* Apparently bacteria have spent their entire history on Earth
>(granted, in your view, that's a much shorter history than in mainstream
>science's view) hiding untold myriads of spare beneficial alleles (and a
>program for calling them forth) in hyperspace, since neither of these show
>up when the bacterial genes are sequenced, but the bacteria keep coming up
>with really weird beneficial adaptions (why should a bacterium have the
>ability to adapt to eat nylon? is this a problem that's likely to come up in
>the natural environment?).
life forms are programmed to adapt to foreign influences, and that
would include stuff that is not likely to come up in the natural
environment.
snip>
>> and how do you determine that what you are observing are mutations
>> from the outside or inherent ability to vary, coming from the inside
>> of the genetic system?
>>
>> It's like watching figures morph in a computer program and claiming
>> that the changes are a result of random external mutations when, all
>> along, the ability to change was programmed into the morphing figures.
>> Have you tracked the source of these changes to determine if they are
>> external or internal?
>>
>Personally, no, though as noted some of these bacterial changes have been
>sequenced. And, again, what on earth would lead a reasonable person to
>suppose that bacteria had a built-in "ability to adapt" (unless that ability
>consisted of the potential to undergo random mutations and natural
>selection) for, e.g. the ability to digest poisons not found in nature?
it is not unreasonable to suppose that a programmer will make his
program with protections from external stimuli that could affect how
the program operates. If a life form is indeed the result of mental
activity, then it is to be expected that built into such a form would
be the ability to protect itself -- a situation that is clearly
evident in how the body's immune system operates, for instance.
snip>
Zoe
<jharshman....@pacbell.net> wrote:
>Zoe wrote:
>
>> On Mon, 01 Aug 2005 05:11:26 GMT, John Harshman
>> <jharshman....@pacbell.net> wrote:
>>
>>
>>>Zoe wrote:
>>>
>>>
>>>>On Mon, 25 Jul 2005 05:02:59 GMT, John Harshman
>>>><jharshman....@pacbell.net> wrote:
>>>>
>>>>snip>
>>>>
>>>>zoe asked:
>>>>
>>>>
>>>>
>>>>>>have they checked the parents of particular offspring and found that
>>>>>>different-numbered genomes were able to interbreed? Or did they
>>>>>>simply test various members, found that some have a certain number
>>>>>>chromosome count, and others a different count, and assumed that
>>>>>>different counts could interbreed?
>>>>>
>>>>>The former. Of course, you understand that you can karyotype individuals
>>>>>and find out if they are hybrids between different chromosome numbers.
>>>>
>>>>
>>>>karyotyping an individual does not tell you that two different
>>>>chromosome-numbered parents interbred. It simply tells you that the
>>>>individual ended up with too many or too few chromosomes. How does
>>>>this happen?
>>>>
>>>>see:
>>>>
>>>>http://gslc.genetics.utah.edu/units/disorders/karyotype/karyotypeinfo.cfm
>>>>
>>>>Quote:
>>>>
>>>>"How can cells end up with too many or too few chromosomes?
>>>>
>>>>"Sometimes chromosomes are incorrectly distributed into the egg or
>>>>sperm cells during meiosis. When this happens, one cell may get two
>>>>copies of a particular chromosome, while another cell gets none."
>>>>
>>>>End quote.
>>>>
>>>>a different count of chromosomes, as seen in karyotyping, does not
>>>>mean that two parents with different counts interbred, but simply that
>>>>the chromosomes got incorrectly distributed during meiosis.
>>>>
>>>>snip>
>>>
>>>I'm afraid all that is irrelevant, since we're not talking about
>>>aneuploidy (which is what the snippet is discussing), but fusions.
>>>Karyotyping can tell you whether the offspring has inherited the unfused
>>>state from one parent and the fused state from another.
>>
>>
>> and on what basis do you decide that a fusion is inherited versus
>> formed during meiosis? Were the parents checked and it was found that
>> one parent had an unfused chromosome and the other had a fused
>> chromosome? Or is this conclusion drawn only from looking at the
>> offspring's chromosomes?
>
>If a particular fusion is polymorphic within a population, surely it's
>much more parsimonious to postulate a single fusion event than a new one
>in each individual.
so this postulation is not a result of observation but of speculation
as to what is more parsimonious?
>Why is this a problem? Your reasoning would make all
>genetic studies invalid.
in what way?
> Why assume that Queen Victoria was the source
>of hemophilia in the royal families of Europe? Couldn't every royal
>hemophiliac have been a unique mutant?
I think you've gotten away from karyotyping. Originally, you seemed
to be saying that karyotyping would be the means of checking to see if
two different-chromosome parents had bred. At least that was the
question I asked, and you answered with your karyotyping example. But
according to the link I gave above, it says that cells end up with too
many or too few chromosomes, not because parents had different
chromosome counts, but because of problems with meiosis. So how did
we get way over here in left field, inspecting poor dead Queen
Victoria's chromosomes?
Zoe
can you provide some reference to your statement here? I remember
reading in Nature back in 2002, after the human genome sequencing was
completed, that it was found (using evolutionary principles of
relationship through DNA sequences) that humans from one part of the
world were more closely related to humans from another part of the
world, than they were to some of their own race or relatives. That,
alone, should disqualify the method as a means of establishing
relationship. I have looked for that particular issue of Nature, but
cannot lay my hands on it. Do you remember reading that article?
> Knowing how descent works is the only means
>that Harshman had at his disposal to identify the various
>members.
but I want to be told, how did John "know" how descent works? It is
this initial "knowing", based on his faulty premise, that is in
question. So I'm not ready to move on to his findings until he
justifies his premise.
> If you have a competing explanation that can produce
>answers bring it to the table, at least table some of the
>exceptions you allude to for discussion.
the same principle of sorting through codons can be applied to
languages other than the genetic language. I am betting that if John
were to put his mind to it, he would be able to tease out some kind of
pattern between computer languages such that some might seem more
closely related than others. And yet common descent would not be a
conclusion in this case.
Here is a (copy and pasted) listing of 145 computer languages. I'm
betting that if you compare these, using similar programs as used for
genetic comparison, you will get patterns that could be interpreted to
mean relationship....except that there is no common ancestor for all
computer languages.
1. ABC
2. ACSL
3. Ada
4. Alef
5. Algol
6. Algol68
7. APL
8. AppleScript
9. Autolisp
10. Awk
11. BASIC
12. BCPL
13. Befunge
14. BETA
15. BLISS
16. BLooP
17. C
18. C#
19. C*
20. C++
21. Cecil
22. CFML
23. CHILL
24. Cilk
25. CLAIRE
26. Clean
27. CLU
28. CMS-2
29. COBOL
30. Common Lisp
31. Concurrent Clean
32. Concurrent Pascal
33. CORAL 66
34. CorelScript
35. csh
36. CSP
37. cT
38. Curry
39. Dylan
40. Dynace
41. Eiffel
42. Elisp
43. Erlang
44. Escher
45. Esterel
46. Euphoria
47. FLooP
48. FORMAC
49. Forms/3
50. Forth
51. FORTRAN
52. FP
53. Goedel
54. GPSS
55. Haskell
56. Hope
57. HyperTalk
58. ICI
59. Icon
60. INTERCAL
61. Interlisp
62. J
63. Java
64. JavaScript
65. Jovial
66. Leda
67. LIFE
68. Limbo
69. Lingo
70. Lisp
71. Logo
72. LotusScript
73. Lua
74. Lucid
75. M
76. Magma
77. Mathematica
78. Mawl
79. Mercury
80. Miranda
81. ML
82. Modula 3
83. Modula-2
84. MUMPS
85. NESL
86. NIAL
87. Oberon
88. Objective-C
89. Obliq
90. occam
91. OPS5
92. Orca
93. Oz
94. Pascal
95. PerfectScript
96. Perl
97. PHP
98. Pict
99. Pike
100. Pilot
101. PL/C
102. PL/I
103. Postscript
104. Prolog
105. Python
106. QBasic
107. Quake-C
108. REBOL
109. Reduce
110. Rexx
111. RPG
112. Ruby
113. S
114. Sather
115. Scheme
116. Self
117. SETL
118. sh
119. Simscript
120. SIMULA
121. Sina
122. SISAL
123. SLAM
124. Smalltalk
125. SML
126. SNOBOL
127. SPARCL
128. SPITBOL
129. T
130. Tcl
131. TECO
132. Telescript
133. Terse
134. TeX
135. Theta
136. Turing
137. UFO
138. Until
139. VBScript
140. VHDL
141. Visual Basic
142. WordBasic
143. xlisp
144. Yorick
145. ZPL
This is one example. Do you need more?
John Harshman
It's hardly speculation. One event is more parsimonious than many.
That's what "parsimonious" means. If one event explains a set of
observations, we prefer that to many events.
>>Why is this a problem? Your reasoning would make all
>>genetic studies invalid.
>
> in what way?
Because we could never suppose that anything had been inherited. It
could always be a new mutation. Genetic studies rely on inheritance.
>>Why assume that Queen Victoria was the source
>>of hemophilia in the royal families of Europe? Couldn't every royal
>>hemophiliac have been a unique mutant?
>
> I think you've gotten away from karyotyping. Originally, you seemed
> to be saying that karyotyping would be the means of checking to see if
> two different-chromosome parents had bred.
Yes. The karyotype of the offspring. Karyotypes are the basic data for
any study of chromosome numbers.
> At least that was the
> question I asked, and you answered with your karyotyping example. But
> according to the link I gave above, it says that cells end up with too
> many or too few chromosomes, not because parents had different
> chromosome counts, but because of problems with meiosis.
And I told you that you the link was talking about aneuploidy, which has
nothing at all to do with chromosome fusion/fission, and thus nothing at
all to do with what we are talking about here.
> So how did
> we get way over here in left field, inspecting poor dead Queen
> Victoria's chromosomes?
Please wait while I count to 10 slowly. OK, back. You want to know why
every instance of chromosomal fusion we observe can't be a new mutation
rather than inheritance from parents. I told you that if we supposed
this, any genetic study would be impossible. Hemophilia in the royal
families of Europe is an example of such a study, one that would be
impossible if we made your assumptions. Instead of tracing the disease
back to Queen Victoria, we would just say that all the hemophiliacs were
new mutants. Now, does that make sense? And forget the aneuploidy; it's
a whole different phenomenon.
Steven J.
"Zoe" <muz...@aol.com> wrote in message
news:79oif1l9d17qe44ck...@4ax.com...
> On Thu, 4 Aug 2005 22:23:34 -0500, "Steven J."
> <sjt195...@nts.link.net.INVALID> wrote:
>
>
> What is the source information for chromosome fission or fusion?
>
> Apparently, the basis on which you decide that the last common
> ancestor was more likely to have 24 chromosomes is because all apes
> except humans have 24 chromosomes. You conclude that there is more of
> a chance for fusion rather fission because there are (present tense)
> more populations of 24's available for the random fusing mutation, and
> less of a chance for the random fissioning mutation to hit a single
> population of 23's. But the probability is calculated on what exists
> today and not on the original population, which is what I think should
> be used.
>
(LCA) of great apes had 23 pairs of chromosomes, then at least three
fissions (of the exact same chromosome, at the exact same place on that
chromosome) had to take place (once in the line leading from the LCA to
orangutans, and once again in the line leading to gorillas after the African
apes split off, and once yet again in the chimp line after the human-chimp
split). Meanwhile, no other chromosomes split or fused in any lineage -- so
why (if the LCA had 24 chromosome pairs) did chromosome 2 split at the same
place in every line except our own? But if the LCA had 24 pairs of
chromosomes, then we only have to account for one fusion in the line leading
to humans after the human-chimp split.
>
> Besides that, I submit that, as an evolutionist, there is no reason to
> reject or accept either scenario since, in principle, evolutionary
> theory starts with a lesser number and evolves into greater numbers,
> anyway.
>
starting at a wall and wandering randomly back and forth. The more time he
wanders, on average, the further he will get from the wall (simply because
he can't get closer to the wall than he was when he started, or go through
it), but any given step or set of steps may take him further from the wall
or further from it (you might want to think of a whole line of drunks, some
staying near the wall, some getting away from it and wandering back, and
others wandering further and further away). The wall represents the minimal
complexity needed to be a living cell (it might be possible for a lineage to
lose that minimal complexity -- but as Darwin pointed out, in a modern,
bacteria-filled world, a lineage that did so wouldn't be a "protocell;" it
would be lunch for the nearest bacterium).
Presumably, if life originated from simpler self-replicating molecules, then
the first life form (ca. four billion years ago) had fewer genes than most
(perhaps any) current species. But evolutionists don't think that evolution
is invariably progressive. Likewise, once complexity has evolved (once a
lineage is far enough away from the "wall" of minimal complexity), it can
perfectly well be lost again: indeed, evolution is replete with examples of
lost complexity (e.g. the hindlimbs of whales, or all the limbs of snakes).
For that matter, what evolutionist typically expect, with regard to number
of parts, is *reduction* of the number of parts, with the remaining parts
becoming more specialized (i.e. a lot of parts that look alike become a
smaller number of parts that look different from each other).
Of course, reducing the number of chromosomes through fusion no more reduces
the number of genes or the amount of "genetic information" than
consolidating three volumes of _Lord of the Rings_ into one makes the novel
shorter.
>
> As well as, there is no predictability. Take, for
> instance,
> a LCA that has 23 chromosomes. It may be probable that a chance
> mutation can come along that causes fission in a chromosome, and a new
> population eventually emerges (according to your theory) where its
> members carry 24 chromosomes.
>
Yes, as far as we know that is perfectly possible. However, to explain the
difference in chromosome numbers among the hominoid (great ape and human)
species through fission, you need, as noted aboe, three fissions in the
exact same place, with no other chromosome fissions or fusions taking place
among the hominoids during that time. That seems rather like bucking the
odds.
>
> And since mutations are
> random, meaning
> that all possible mutations have equal probability of selection, then
> humans (according to your theory) could have descended from the
> original population that had 23 chromosomes, and the population with
> the new 24th chromosome, through geographical isolation (according to
> your theory) could be hit with other mutations (according to your
> theory) that would cause the first 24-chromosome population to
> continue to vary into your gorillas and other ape types (according to
> your theory).
>
Yes, *if* we had no idea of the order in which the various hominoid lineages
split off from one another, you would be correct. If it were reasonable to
accept common descent, but assume that, e.g. oranguatans were more closely
related to chimps than we are, then yes, a fission would be as "likely" an
explanation as a fusion (aside from the vestigial telomere and centromere in
chromosome 2)..
The trouble is, genetic sequences strongly indicate that gorillas split off
from the chimp-human line *before* chimps and humans split from each other.
And, of course, oranguatans are even more different, and therefore (it is
inferred) split off from the line leading to African apes before the
human-gorilla split. This is why I didn't bring up bonobos (pygmy
chimps): they also have 24 chromosome pairs, but they split off from chimps
after chimps split off from us, so if a chromosome fission took place early
in the chimp line (after it split from humans) it could be easily inherited
by both species. If you count in all the great ape species (not just the
splits that occurred between the great ape-lesser ape split and the
human-chimp split), then species with 24 pairs outnumber those with 23 pairs
by about six to one, not three to one -- but those splits that took place
after the human-chimp LCA don't "count" for this purpose.
By the way, while I don't think it's important to this discussion,
"mutations are random" does *NOT* mean "all mutations are equally likely,"
or "all mutations are equally likely to be selected" (while there's no
reason to believe fusions are more likely to become fixed in a population
than fissions, if they *were* more likely to be fixed, it would not mean
that these sorts of mutations were not random). "Random" means simply that
whatever causes mutations is not related to whatever causes mutations to be
beneficial, harmful, or neutral.
>
-- [large snip]
>
>>I suspect you're asking me for a mutation by mutation, selective regime by
>>selective regime, account of how the human digestive tract evolved from a
>>single-celled organism. I cannot, of course, provide any such thing.
>
> and why not? Based on your scientific, observed data of how mutations
> behave, surely you can plug that data into your evolutionary scenario
> and scientific observations of how mutations and selection work in
> describing a realistic step-by-step pathway on how a digestive system
> can come into existence. If you can't do this, then I must take your
> declaration on faith...which I am not inclined to do.
>
>> I
>>also suspect that you have neither the intention nor the ability to tell
>>us
>>how "intelligence" (other, perhaps, than human intelligence) implements
>>any
>>"design" or change in design in living organisms.
>
> I cannot make a digestive system, so I cannot tell you how to do it.
> But if I were to try to recreate something that works like the
> digestive system, I certainly would not try to do it by random
> mutations. Would you? I would take note of the steps taken in a
> what-you-see-is-what-you-get system, and attempt to copy those, as far
> as possible. And that would be a useful, scientific venture, learning
> from nature, copying its processes, rather than speculating on its
> history.
>
Why would you not use random mutations? If you don't know how to make a
digestive system, making lots of copies of an initial cell, varying them in
small ways, and seeing which ways move you closer to a digestive system,
might be a better idea than trying to dream up a complete digestive system
from scratch. Note that, before there are any digestive systems, you can't
very well copy one that already exists (since none do).
Note that developmental biologists are attempting to learn from nature and
discover the processes at work (why copy them? we already have digestive
systems). As yet, only the broad outlines and a few isolated details of how
genes and the other molecular systems in a cell build an organism are well
understood; the exact number of genes in a human or chimp has not been
counted yet, and still less is the exact function of all those genes (many
still unknown) discovered.
>
>>> So, okay, we have a simple common ancestor consisting of a single
>>> functioning cell (and even that is a generous given) that replicates
>>> (we know not how that started). Take it from there and describe a
>>> realistic scenario, using factual, scientific observations, as to how
>>> this single cell develops a digestive system, based on random
>>> mutations and selection.
>>>
>>> Can't do it? Then evolutionists need to be a little humbler about
>>> their position. To say "We know the digestive system evolved," but go
>>> silent when the question of "how?" is asked, is to ask thinking minds
>>> to take your word on faith.
>>>
>>Don't be silly, Zoe. It is perfectly possible to demonstrate that
>>something
>>happened, without having a complete description of how it happened. Your
>>position is tantamount to saying that if we can't figure out how someone
>>died, we are not justified in inferring that he is dead.
>
> the issue is not about whether someone is dead or whether something
> happened. It is about HOW something happened. My position is
> tantamount to saying that if we can't figure out how someone died, we
> are not justified in making up stories about how he died. There is no
> controversy over whether the person is dead. Neither is there
> controversy that we exist.
>
One of the things that have been inferred to have happened is common
descent.
>
>>You have, in the consistent nested hierarchy of homologies,
>
> you have yet to demonstrate that nested hierarchies always mean common
> descent. If they do not always mean common descent, then on what
> basis do you decide that only the nested hierarchies of nature mean
> common descent?
>
I have argued that *consistent* nested hierarchies -- seen if families of
hand-copied manuscripts, families of languages, and clades of living
organisms -- imply common descent. Your supposed counterexamples involve
sets of entities that fall into very different hierarchies depending on what
traits one chooses to examine and compare.
>
>> in biogeography,
>
> why does biogeography mean common descent, unless there is a
> preconceived notion in place?
>
If, e.g. the various genera of the hominoids are not related, why do the two
living genera most genetically similar to humans share a continent with [a]
the greatest genetic diversity of humans (indicating humans have lived on
that continent longer than they've lived on other continenets), and [b] with
the australopiths, the extinct great ape genus most similar to our own genus
_Homo_. On the assumption of separate creation, gorillas might as well be
in Asia along with orangutans -- or even in Central America alongside howler
monkeys. Separate origins offers no reason for similar "kinds" to be found
in the same geological region as one another or extinct "kinds" similar to
them.
>
>>in vestigial structures at the genetic and morphological level,
>
> the term "vestigial structures" is a term arising out of preconceived
> notions. Some may call the appendix vestigial, but there are uses for
> the appendix. Some may call the tailbone vestigial, but there are
> uses for the tailbone...and so on. To call something vestigial
> because it seems to have no use is a misunderstanding of and
> egotistical dismissal of structures that are really not vestigial at
> all.
>
"Vestigial structures" are defined as having *reduced* function, not *no*
function, and can be recognized without regard to evolutionary notions.
Indeed, they can be recognized where evolution is rejected as an
explanation: the shortened simplified limbs of a thalidomide baby are
vestigial according to definition (that is, they lack some of the function
of homologous structures in related or allied organisms), but the vestigial
limbs aren't caused by any genetic change (the genes are unchanged), and
therefore cannot be an example of evolution. However, when vestigial
features are not the result of developmental derangement, it is reasonable
to ask why they share so many details of structure with organs with which
they do not share details of function, in species otherwise very similar to
the one with the vestigial structure.
Saying that the appendix is vestigial does not mean it does nothing; it
means that it occupies the location and shares embryological and anatomical
features with the caecum, a pouch used to digest leaves in many monkeys.
Since it doesn't digest leaves in humans, why does it have this location and
these traits? Why does the human tailbone, whatever its uses, share so many
homologies to actual tails in other primates (and other mammals)? Vestigial
structures are simply an extreme case of the problem of "parahomology:"
similar designs for dissimilar functions. It's one thing to use commn
design for common purposes, but what logic (other than evolutionary logic,
in which the function of a structure can evolve over time, without erasing
all traces of the structure's history) is there to common design for
different purposes (especially when there is also -- consider bat, bird, and
pterosaur wings -- different design for common purposes).
>
>> in the
>>fossil record,
>
> the fossil record is subject to interpretation.
>
Yes, and when some creationists say that ER1470 is "fully human" and others
say it is "fully ape," then something is wrong with the creationist
interpretation (that all fossils are fully one "kind" or another, with no
intermediates) can possibly be correct.
>
>>in the jury-rigged and improvised nature of many adaptions
>>(e.g. Darwin's remark on "similar structures for dissimilar functions and
>>dissimilar structures for similar functions"), compelling evidence for
>>common descent with modification.
>
> nothing compelling so far to this creationist.
>
>>You have, furthermore, an demonstrated mechanism of mutation and natural
>>selection.
>
> this is a mechanism that fails to produce a digestive system, so how
> has it been demonstrated? Instead, you want your systems to be fully
> in place and operating a la creation, and then you begin to apply your
> theory of random mutations to these ready-made systems. You can't
> have this head start unless you acknowledge that the system was in
> place, fully functioning, from the beginning -- which is the position
> of creation theory.
>
There is no creation theory, and your ramblings have not changed that.
There was a creation theory once. It predicted that no genus would ever go
extinct, that human artifacts would turn up under the lowest level of
sediments, and that scientific dating methods would show the Earth to be
thousands of years old. After all of these predictions failed, creation
theory was replaced with the assertion that evidence means nothing, if it
contradicts religious dogma, because God could have created the world and
subsequently intervened in it in any manner that struck His fancy.
Elaborating this position with every "god of the gaps" argument that springs
to mind does not make creationism a theory.
And you, please note, have not demonstrated that natural selection of
mutations "fails" to produce a digestive system. Above, you argue that we
cannot assert that some structures are functionless "junk" because we don't
know all the details of how biology works. Here, you seem to ignore you own
point and argue that we know so much about all the details of biology that
if it were possible to give a mutation-by-mutation, selective
regime-by-selective regime evolutionary history of the digestive tract, any
supporter of mainstream science could pull one out of his hat. I do not
think you can logically adhere to both positions at once.
>
>> It has produced, in the lab, bacteria resistant to poisons never
>>found in nature,
>
> the ability to respond to changes in the environment, including
> poisons never found in nature, is an inherent ability.
>
Zoe, you are being obstinate here. You are simply assuming that you, in
abject ignorance of biology, know more about how living things work that
thousands of scientists who've spend decades studying these systems.
>
>> bacteria that *eat* poisons never found in nature,
>
> as long as the bacterium is programmed to respond to alien influences,
> including poisons never found in nature, it will adapt to these alien
> influences, or die, depending on its health.
>
You are wrong. You are stringing words together and mistaking this for an
argument.
>
>>multicellular colonial organisms evolved from single-celled ancestors,
>
> I submit you are observing a programmed ability to divde, and are
> mistakenly calling it evolution.
>
>> and
>>similar examples of striking novel traits. It seems to me that you are
>>not
>>being asked to accept anything on "faith," but on the basis of
>>considerable
>>evidence regarding both the fact and the proposed mechanism for it.
>
> faith is called upon to rely on your interpretation of the above data,
> Steven.
>
>>> So, here we go.
>>>
>>> A single cell exists, replicating itself repeatedly. Along comes a
>>> random "beneficial mutation." What happens next, based on your
>>> selection principle? How does the digestive system develop?
>>>
>>It becomes a multicellular organism.
>
> could you be a little less vague? So you think that a single cell
> becoming multicellular is how a digestive system forms? Have you
> accounted for the changes in DNA sequences that are needed to produce
> the particular types of proteins needed to construct an esophagus, a
> stomach, duodenum, jejunum, small intestines, and all the attendant
> parts that make a digestive system work?
>
Multicellularity preceeds specialization of the cells in question. For that
matter, formation of a digestive system preceeds all those specialized
subcomponents you mention.
>>I am not; please read more carefully. I am stating that if mtDNA
>>differences are so tiny, then presumably nuclear DNA differences are even
>>smaller, so that two dogs can be 99.8% or more genetically identical, and
>>be
>>as morphologically different as chihuahuas and St. Bernards.
>
> this is an assumption without foundation. Just because mtDNA
> differences are tiny, there is no reason to presume (your word),
> without evidence, that nuclear DNA differences are even smaller.
> Indeed, as mentioned earlier, after chimp/human genome comparison, it
> has been noted that the differences are 83%, so definitely not
> smaller.
>
I would assume this on the evidence that mtDNA differences are larger than
nuclear DNA differences both within species (e.g. humans) and between
species (e.g. humans and chimps). This is pretty much common knowledge.
Again, you seem to be confusing percentage of sequence similarity with the
percentage of genes that have some difference. Having 83% of *genes*
different is not the same as having 83% of the sequence of nucleotides
different, and indeed one could in principle have 99% sequence similarity,
with 100% of genes each being 1% different in the two species. If you don't
understand this, what in this discussion are you capable of understanding?
>
>>-- [snip]
>>
>>Let me reargue this entire section (i.e. my assertion that major changes
>>in
>>DNA sequence can have little or no effect on morphology).
>>
>>The genetic code (the correspondence of three-nucleotide codons to amino
>>acids that make up proteins) is "degenerate:" rather than having one codon
>>per amino acid and one for punctuation, most amino acids correspond to
>>multiple codons (up to six), and there are three separate stop codons.
>>From
>>this it follows that one could, in principle, make massive changes (ca.
>>30%
>>of the sequence) in the genome of any species without making any changes
>>at
>>all in the proteins produced or the way the organism grows.
>
> I'm not sure what you mean by "massive" here. That these codons allow
> for the morphing of a species into another? What exactly are these
> massive changes?
>
Zoe, as a rule, when I include a parentheses that says "ca. 30% of the
sequence" after "massive," you are justified in assuming I meant, by
"massive," "about 30% of the sequence." This is far greater than the
sequence difference between humans and, say, monkeys. And when I say that
these changes could be made "without making any changes at all in the
proteins produced or the way the organism grows," I thought you would deduce
that, in fact, the species would not "morph" at all, even though the genetic
changes are larger than those separating dogs from cats.
>
>> This are
>>"silent mutations" -- they have no phenotypic effects at all. Therefore,
>>logically, one cannot assume that changes in the genome must translate to
>>changes in the phenotype at all, much less must map one-for-one onto the
>>changes in the phenotype.
>
> these variations of codons for protein don't vary the proteins to the
> point where you have change in morphology, so why use them as evidence
> at all then?
>
We were discussing whether 98.4% sequence similarity had to mean 98.4
percent morphological similarity. There are two aspects to that question:
do tiny changes in the genome automatically mean tiny changes in the
organism, and do large changes in the genome automatically mean large
changes in the organism. We were discussing, above, the latter point.
>
-- [snip]
>
>>The issue is not whether the flies can successfully reproduce
>
> it most certainly is the issue. You are asserting that changes such
> as seen done in the fruit fly are evidence for evolution of the
> species. If the flies cannot successfully reproduce, then you don't
> have a species that can continue to morph. End of the line. No
> macroevolution along that fruit-fly line.
>
No, we are discussing what different forms of the same gene can do, as part
of an attempt to show you that large changes in the genome do not have to
mean large changes in the phenotype. Can the human gene do the same job as
the fly gene, even though it is not identical to the fly gene? If it can
trigger eye development, there is reason to suppose it can.
>
-- [snip]
>
>>First of all, my argument does not depend on the assumption that the
>>differences between, e.g. human and pine tree cytochrome-c evolved in the
>>course of descent from a common ancestor. It depends only on the
>>assumption
>>that human and pine tree cytochrome-c do the same job, engaging in the
>>same
>>chemical reactions.
>
> it makes sense, based on the behavior of creative mental activity,
> that a particular gene would be used in the master plan for all life
> forms, but switched on for some life forms and switched off for other
> life forms. When switched off, it is not even recognizable as a gene,
> but is just part of the material that is presently called junk. Why
> switch this gene off? I might want to give certain life forms the
> ability to enjoy citrus fruit and therefore switch off that gene so
> that there is not an overload of vitamin C?
>
No, Zoe, genes are recognizable as genes whether they are "turned on" or
not. And, by the way, we were discussing cytochrome-c, not the GULO
pseudogene (which I think is not found in pine trees).
>
>> If this is correct, a mutation or series of mutations
>>which did change human cytochrome-c to pine tree cytochrome-c would not
>>alter the way our metabolisms worked or our morphology. That is, not only
>>can silent mutations produce, in principle, large changes in DNA with no
>>changes in phenotype, even non-silent mutations could produce very tiny,
>>inconsequential changes in phenotype. This was one of the points under
>>contention.
>
> meaning you can have it working for you all ways, coming and going --
> sounds very much like a sweeping "mutationsdidit" with no further
> explanation.
>>
>>By the way, even if you don't accept (or, I suspect, understand) the
>>argument about consistent nested hierarchies as evidence for common
>>descent,
>>at least you could acknowledge that it has been presented to you. The ant
>>in your little parable offers no argument, not even a bad one, for cars
>>evolving into aircraft or for the common ancestry of cars and aircraft (of
>>course, cars and aircraft reproduce rather differently from living
>>things).
>
> the ant is an apt example of human thinking in relation to the things
> we don't understand. The ant might think, if it could think, that it
> has a great argument for how a car changes into an airplane. It is an
> ant's perspective. Relatively speaking, humans are like ants.
>
Frankly, I'm beginning to think I could have a more productive discussion of
evolution with an ant.
>
-- [snip]
>
-- Steven J.
Eric Rowley
> On Sat, 6 Aug 2005 00:13:48 -0400 (EDT), B Richardson
> <br...@nym.hush.com> wrote:
<snipalot>
> > Knowing how descent works is the only means
> >that Harshman had at his disposal to identify the various
> >members.
> but I want to be told, how did John "know" how descent works?
It has been studied by biologists for hundreds of years.
In this case however I think that "how descent works" is
more background knowledge, what specifically enabled him to
solve the problem was his prior knowledge of the shape
of the family tree of primates. The whole point was to
demonstrate that any large enough section of DNA will produce
the same tree.
> It is this initial "knowing", based on his faulty premise,
What premise do you think is faulty?
> that is in question. So I'm not ready to move on to his findings
> until he justifies his premise.
> > If you have a competing explanation that can produce answers
> >bring it to the table, at least table some of the
> >exceptions you allude to for discussion.
> the same principle of sorting through codons can be applied to
> languages other than the genetic language.
Certainly, fsvo "codon".
At lot of work has been done on the family tree of human
languages for instance.
Or family trees, as the case may be, but I understand that
at least some linguists think that all languages are related.
> I am betting that if
> John were to put his mind to it, he would be able to tease out
> some kind of pattern between computer languages such that some
> might seem more closely related than others.
What do you meen "seem"?
What on earth makes you think that computer languages _aren't_
related by descent?
If someone thinks they need a new programing language they
in most cases won't make it up from scratch, rather they
will look around for a language that is close to what they
think they need and modify it.
See http://www.levenez.com/unix/history.html#06 for a small ;-)
portion of the family tree of computer languages, variants of
Unix and Linux.
Note that it is messier than, at least, the multicellular
portion of the tree of life because the language developers
sometimes combine features from two or more separate languages
into their new language so that there are crosslinks where
the branches come together again.
> And yet common
> descent would not be a conclusion in this case.
It most certainly would, at least within language families.
> Here is a (copy and pasted) listing of 145 computer languages.
> I'm betting that if you compare these, using similar programs as
> used for genetic comparison, you will get patterns that could be
> interpreted to mean relationship....except that there is no
> common ancestor for all computer languages.
It doesn't really matter whether there is a _single_ common
ancestor for _all_ languages, if different language families
have separate origins then we would end up with several
separate trees, one for each separate group.
But if everything comes together in a single consistant tree,
like the tree of life, then that is very strong evidence for
a single common origin.
Note that the english language could be considered
a common ancestor for a large group of computer
languages.
Others are based mainly on the "language" of mathematical
and logical symbols.
<snip list>
> This is one example.
No it isn't, this is a case where the nested hierarchy,
as far as it exists, _is_ due to common descent.
> Do you need more?
Yes please.
Eric
John Harshman
I certainly don't. And given your track record on this it's almost
certain that if it exists you have seriously garbled what it said.
>>Knowing how descent works is the only means
>>that Harshman had at his disposal to identify the various
>>members.
>
> but I want to be told, how did John "know" how descent works? It is
> this initial "knowing", based on his faulty premise, that is in
> question. So I'm not ready to move on to his findings until he
> justifies his premise.
The premise is simpler than any idea of how evolution works; it's simply
the claim that analysis of any gene will give us the same tree of
primate relationships. As you see, that premise turns out to be true.
Now the question is why that premise turns out to be true. How do you
explain it?
>>If you have a competing explanation that can produce
>>answers bring it to the table, at least table some of the
>>exceptions you allude to for discussion.
>
> the same principle of sorting through codons can be applied to
> languages other than the genetic language. I am betting that if John
> were to put his mind to it, he would be able to tease out some kind of
> pattern between computer languages such that some might seem more
> closely related than others. And yet common descent would not be a
> conclusion in this case.
You have no doubt. But I don't think you are right. Instead of nonsense
examples, try dealing with the actual question. How does it happen that
whatever gene you look at, you get the same tree of primate
relationships? Do you still contend that this is arbitrary? If so, how
do you explain the multiple, identical results from different data? If
it's not arbitrary, what causes this phenomenon?
> Here is a (copy and pasted) listing of 145 computer languages. I'm
> betting that if you compare these, using similar programs as used for
> genetic comparison, you will get patterns that could be interpreted to
> mean relationship....except that there is no common ancestor for all
> computer languages.
It's a nice list, but I have no idea what I'm supposed to do with them,
or how you would go about comparing them. I'll make a bet too: I bet
that you could come up with dozens of mutually exclusive classifications
of all these languages, based on different features. You will not find,
as we did with primates, that classifications based on different
features give you the same answer.
Interestingly, classification of natural languages is easier, and
methods similar to what I use give us consistent trees. Since we know
that natural languages have indeed evolved by branching, that suggests
that the tree-making methods are valid.
I will note also that there is some degree of inheritance among computer
languages, i.e. c++ is partly a descendant of c and inherits some of its
structures from c; in that way it's clearly more closely related to c
than to pascal. Similarly, BASIC is in many ways a descendant of
FORTRAN. These are real genealogical relationships, real inheritance.
However, extensive horizontal transfer destroys most relationships.
> This is one example. Do you need more?
Sure. Tell us about the sweaters again. The problem is that you don't
know the difference between arbitrary and natural classifications. Look
at the primate data: no matter what you do, you get the same tree. You
can't possibly make the same claim for any of your little examples.
B Richardson
All kinds of pet projects are going on.
http://freepages.genealogy.rootsweb.com/~allpoms/genetics1a.html
I only looked at a couple. I liked this one:
http://www.roperld.com/ycomparison.htm#37Markers
He used the same tool I used in the second part of our
excercise.
> I remember
>reading in Nature back in 2002, after the human genome sequencing was
>completed, that it was found (using evolutionary principles of
>relationship through DNA sequences) that humans from one part of the
>world were more closely related to humans from another part of the
>world, than they were to some of their own race or relatives. That,
>alone, should disqualify the method as a means of establishing
>relationship. I have looked for that particular issue of Nature, but
>cannot lay my hands on it. Do you remember reading that article?
>
No.
>
>> Knowing how descent works is the only means
>>that Harshman had at his disposal to identify the various
>>members.
>
>but I want to be told, how did John "know" how descent works? It is
>this initial "knowing", based on his faulty premise, that is in
>question. So I'm not ready to move on to his findings until he
>justifies his premise.
>
When things are copied and errors occur, the replicated copies
inherit those errors. You find a unique fingerprint in the
errors when all the descendants are examined.
The simplest way I can think of to explore this principle
to take a simple text string of your choosing, make a
couple of copies, introduce errors into the copies,
make copies of the copies, and introduce errors into those
copies and look over what you got. See if you can see
anything in the inherited errors in a string that may
indicate which string it was copied from, and which string
its parent was copied from. You can make a branch by
making two copies of a string and introducing different
errors into their respective descendants.
>
>> If you have a competing explanation that can produce
>>answers bring it to the table, at least table some of the
>>exceptions you allude to for discussion.
>
>the same principle of sorting through codons can be applied to
>languages other than the genetic language. I am betting that if John
>were to put his mind to it, he would be able to tease out some kind of
>pattern between computer languages such that some might seem more
>closely related than others. And yet common descent would not be a
>conclusion in this case.
He surely could. As could probably you, I and most others.
We also would likely all come up with wildly varying (though
possibly meaningful) ways to classify them in a hierarchical way.
>
>Here is a (copy and pasted) listing of 145 computer languages. I'm
>betting that if you compare these, using similar programs as used for
>genetic comparison, you will get patterns that could be interpreted to
>mean relationship....except that there is no common ancestor for all
>computer languages.
>
>From the group I have chosen Autolisp , Awk, csh, CSP, and Floop,
and categorized them on a criterion.
How would you match them up on the tree?:
|-------A4
|---+
| |-------A5
+
| |---A2
| |---+
| | |---A3
|---+
|-------A1
See what I mean? There's all sorts of meaningful ways to
organize them, but subjective and not consistant. Without
knowledge of the details I used to categorize them, the only
ways to come up with the same tree as I did is by chance, or by
selectively applying knowledge you have about those languages
until you get the same tree. Harshman identified which species
the nucleotides I posted belonged to *without* using any
detailed knowledge of the species themselves, and I concealed
information about which was which. In part two of the excercise John
didn't even have the nucleotides, I just created a tree using the
nucleotides using the same tool that is being used at
http://www.roperld.com/ycomparison.htm#37Markers
That was also my first use of the tool, I'm a layperson
like you and not a scientist like John or Steven J. So
how were we able to pull this off? We certainly can't do
this with computer languages or sweaters without corroborating
amongst ourselves. What's more, if had accidently mixed up
Colobus and Pongo and disputed Harshman's matchings, an examination
of my files by a neutral third party would have shown the error
to be mine.
>[snipped to reduce linecount]
>
>This is one example. Do you need more?
>
Sure, I don't see that the example you gave has any meaningful
parallels.
Zoe
<sjt195...@nts.link.net.INVALID> wrote:
zoe asked:
>> What is the source information for chromosome fission or fusion?
>>
>> Apparently, the basis on which you decide that the last common
>> ancestor was more likely to have 24 chromosomes is because all apes
>> except humans have 24 chromosomes. You conclude that there is more of
>> a chance for fusion rather fission because there are (present tense)
>> more populations of 24's available for the random fusing mutation, and
>> less of a chance for the random fissioning mutation to hit a single
>> population of 23's. But the probability is calculated on what exists
>> today and not on the original population, which is what I think should
>> be used.
>No, that is not the basis. The basis is this: if the last common ancestor
>(LCA) of great apes had 23 pairs of chromosomes, then at least three
>fissions (of the exact same chromosome, at the exact same place on that
>chromosome) had to take place (once in the line leading from the LCA to
>orangutans, and once again in the line leading to gorillas after the African
>apes split off, and once yet again in the chimp line after the human-chimp
>split).
why would there have to be three fissions? You're forgetting about
inheritance. You can have a member of a 23-chromosome population get
hit by your mutation, supposedly causing fission. That member should
now be the LCA of populations with 24 chromosomes. If the first small
population of 24's does not get decimated by the abundance of 23's
(most likely to happen within your worldview), then you now have your
growing population of 24's which, according to your theory,
differentiated into gorillas, chimps, et cetera.
If you insist that the 24-chromosome population was more likely to
start first, then you still have to explain how the first 24's
differentiated into your hypothesized various species of apes. Your
explanation for this differentiation could have taken place just as
well before a fusion occurs, as after a fission occurs. It has
nothing to do with parsimony.
So I don't see how probability and statistics has an answer to
something that you have no idea which came first, 23 or 24. How can
odds be placed on an unknown? It is not known if your "history" of
ape chromosomes is even a reality. It's like saying, let's suppose
that fairies exist and they have a human-like form. Now we can
sequence DNA from humans and then we'll know what fairies' DNA was
like.
large snip of non-answers>
>By the way, while I don't think it's important to this discussion,
>"mutations are random" does *NOT* mean "all mutations are equally likely,"
>or "all mutations are equally likely to be selected"
isn't that the meaning of "random"? Why the specialized meaning of
random in evolutionary theory then? Might as well use a different
term.
snip>
>>>also suspect that you have neither the intention nor the ability to tell
>>>us
>>>how "intelligence" (other, perhaps, than human intelligence) implements
>>>any
>>>"design" or change in design in living organisms.
>>
>> I cannot make a digestive system, so I cannot tell you how to do it.
>> But if I were to try to recreate something that works like the
>> digestive system, I certainly would not try to do it by random
>> mutations. Would you? I would take note of the steps taken in a
>> what-you-see-is-what-you-get system, and attempt to copy those, as far
>> as possible. And that would be a useful, scientific venture, learning
>> from nature, copying its processes, rather than speculating on its
>> history.
>>
>Why would you not use random mutations?
would you? Observation of how mental activity behaves in the real
world would tell you that things are not constructed through random
activity. So if creation theory contends that the digestive system is
not the result of random activity, this contention correlates well
with how mental activity behaves.
> If you don't know how to make a
>digestive system, making lots of copies of an initial cell, varying them in
>small ways, and seeing which ways move you closer to a digestive system,
>might be a better idea than trying to dream up a complete digestive system
>from scratch.
trial and error is a tool of mental activity if a creator has not yet
figured out how to make something. But unlike random mutations that
have no idea that they want to make a digestive system, mental
activity knows what it wants to make, and it plans and dreams and
works towards its goal.
> Note that, before there are any digestive systems, you can't
>very well copy one that already exists (since none do).
my mention of copying had to do with how a creationist would approach
science. They would copy nature, and learn how to use the principles
seen in nature to create new things.
But back before digestive systems existed on this earth, if you had to
make a digestive system from scratch, I would hope you would put your
mind to the task and figure out how best to approach it. You'd be
fired on your first day on the job if you were caught sitting around
idly doodling on your pad, hoping that something would come together
on its own....which is the principle upon which evolutionary theory is
based.
snip>
>>>You have, in the consistent nested hierarchy of homologies,
>>
>> you have yet to demonstrate that nested hierarchies always mean common
>> descent. If they do not always mean common descent, then on what
>> basis do you decide that only the nested hierarchies of nature mean
>> common descent?
>>
>I have argued that *consistent* nested hierarchies -- seen if families of
>hand-copied manuscripts, families of languages, and clades of living
>organisms -- imply common descent. Your supposed counterexamples involve
>sets of entities that fall into very different hierarchies depending on what
>traits one chooses to examine and compare.
there's the key: "Depending on what traits one chooses to examine and
compare."
Families of languages would not fall into a nested hierarchy if you
chose other traits for comparison than the ones you have chosen to
use. Those same languages that seem to fall into a nested hierarchy
would not appear hierarchical if you chose to classify them according
to other traits.
Depending on the traits you choose to use for comparison you can get a
nested hierarchy and even twin or triple-nested hierarchy, or none --
all for the same groups.
>>> in biogeography,
>>
>> why does biogeography mean common descent, unless there is a
>> preconceived notion in place?
>>
>If, e.g. the various genera of the hominoids are not related, why do the two
>living genera most genetically similar to humans share a continent with [a]
>the greatest genetic diversity of humans (indicating humans have lived on
>that continent longer than they've lived on other continenets), and [b] with
>the australopiths, the extinct great ape genus most similar to our own genus
>_Homo_.
this, again, is the as-yet-unsupported premise that similarity means
relationship. On what basis do you decide that similarity must means
relationship for only biological life forms, but nowhere else? So
far, this question has not been answered by anyone.
snip>
>>>in vestigial structures at the genetic and morphological level,
>>
>> the term "vestigial structures" is a term arising out of preconceived
>> notions. Some may call the appendix vestigial, but there are uses for
>> the appendix. Some may call the tailbone vestigial, but there are
>> uses for the tailbone...and so on. To call something vestigial
>> because it seems to have no use is a misunderstanding of and
>> egotistical dismissal of structures that are really not vestigial at
>> all.
>>
>"Vestigial structures" are defined as having *reduced* function, not *no*
>function, and can be recognized without regard to evolutionary notions.
and what is the standard for reduced function? You have to first
know the function of the supposed "vestige" in order to say its
function has been reduced. It's too superficial to look at a
similar-looking organ in another life form and decide that, therefore,
this "vestigial" organ is indeed meant to function the same way as the
other, but it's just not functioning anymore.
You might as well look at the trunk of a car and call it vestigial
because the tray of a pickup truck seems to perform a similar
function, just more extensively.
>Indeed, they can be recognized where evolution is rejected as an
>explanation: the shortened simplified limbs of a thalidomide baby are
>vestigial according to definition (that is, they lack some of the function
>of homologous structures in related or allied organisms), but the vestigial
>limbs aren't caused by any genetic change (the genes are unchanged), and
>therefore cannot be an example of evolution. However, when vestigial
>features are not the result of developmental derangement, it is reasonable
>to ask why they share so many details of structure with organs with which
>they do not share details of function, in species otherwise very similar to
>the one with the vestigial structure.
human creators use the same template for many different purposes. If
mental activity is evidenced in the use of templates, why doesn't the
similarity of structures not cause you to see mental activity here,
also?
>Saying that the appendix is vestigial does not mean it does nothing; it
>means that it occupies the location and shares embryological and anatomical
>features with the caecum, a pouch used to digest leaves in many monkeys.
no, no, no. The cecum or caecum in the monkey has its counterpart in
the cecum or caecum of the human. Its counterpart is NOT the
appendix. See:
http://en.wikipedia.org/wiki/Caecum
"Cecum or caecum is a pouch connected to the large intestine between
the ileum and the colon. It is separated from the ileum by the
ileocecal valve (ICV) or Bauhin's valve, and is considered to be the
beginning of the large intestine and part of the colon.
"Its primary function is to absorb water and salts from undigested
food. It has a muscular wall that can knead the contents to enhance
absorption.
"The cecum is present in mammals, birds, and some reptiles."
>Since it doesn't digest leaves in humans, why does it have this location and
>these traits?
the appendix is not even designed to have supposedly digested leaves.
It has a lymphatic function and seems well placed in an area that most
needs it.
See:
http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Lymphoma?OpenDocument
"The lymphatic system is part of the immune system, which defends the
body against infection. It consists of lymph nodes connected by lymph
vessels, which branch out into all parts of the body except the brain
and spinal cord. The lymphatic system also includes the bone marrow,
spleen, thymus gland, tonsils, adenoids and APPENDIX (caps mine.)"
What better area to place an organ of the lymphatic system than at a
point where bacteria are likely to be present?
> Why does the human tailbone, whatever its uses, share so many
>homologies to actual tails in other primates (and other mammals)?
based on how mental activity behaves, it is evident that a successful
template works for many different purposes.
> Vestigial
>structures are simply an extreme case of the problem of "parahomology:"
>similar designs for dissimilar functions. It's one thing to use commn
>design for common purposes, but what logic (other than evolutionary logic,
>in which the function of a structure can evolve over time, without erasing
>all traces of the structure's history) is there to common design for
>different purposes (especially when there is also -- consider bat, bird, and
>pterosaur wings -- different design for common purposes).
I suggest a study of how mental activity behaves when creating items,
and you will get your answer as to common design for different
purposes and different design for common purposes.
Reducing this to basics, a rectangle is a common design used for many
different purposes. Or a circle is a different design for common
purposes.
snip meanderings>
>>>> A single cell exists, replicating itself repeatedly. Along comes a
>>>> random "beneficial mutation." What happens next, based on your
>>>> selection principle? How does the digestive system develop?
>>>>
>>>It becomes a multicellular organism.
>>
>> could you be a little less vague? So you think that a single cell
>> becoming multicellular is how a digestive system forms? Have you
>> accounted for the changes in DNA sequences that are needed to produce
>> the particular types of proteins needed to construct an esophagus, a
>> stomach, duodenum, jejunum, small intestines, and all the attendant
>> parts that make a digestive system work?
>>
>Multicellularity preceeds specialization of the cells in question. For that
>matter, formation of a digestive system preceeds all those specialized
>subcomponents you mention.
I'm afraid that formation of an overarching system to hold a digestive
system precedes even the digestive system, not to mention the
specialized subcomponents.
<snip inability to explain how selected mutations cause evolution>
Zoe
snip>
>>>If a particular fusion is polymorphic within a population, surely it's
>>>much more parsimonious to postulate a single fusion event than a new one
>>>in each individual.
>>
>>
>> so this postulation is not a result of observation but of speculation
>> as to what is more parsimonious?
>
>It's hardly speculation. One event is more parsimonious than many.
>That's what "parsimonious" means. If one event explains a set of
>observations, we prefer that to many events.
science is not about what is preferred but about what IS. In an area
where the history is absent, the preference for parsimony does not
produce evidence other than "it feels better this way."
snip>
>>>Why assume that Queen Victoria was the source
>>>of hemophilia in the royal families of Europe? Couldn't every royal
>>>hemophiliac have been a unique mutant?
>>
>> I think you've gotten away from karyotyping. Originally, you seemed
>> to be saying that karyotyping would be the means of checking to see if
>> two different-chromosome parents had bred.
>
>Yes. The karyotype of the offspring. Karyotypes are the basic data for
>any study of chromosome numbers.
>
>> At least that was the
>> question I asked, and you answered with your karyotyping example. But
>> according to the link I gave above, it says that cells end up with too
>> many or too few chromosomes, not because parents had different
>> chromosome counts, but because of problems with meiosis.
>
>And I told you that you the link was talking about aneuploidy, which has
>nothing at all to do with chromosome fusion/fission, and thus nothing at
>all to do with what we are talking about here.
the link talks about karyotyping, which is what you offered as your
evidence that two parents carried different chromosomes.
>> So how did
>> we get way over here in left field, inspecting poor dead Queen
>> Victoria's chromosomes?
>
>Please wait while I count to 10 slowly. OK, back. You want to know why
>every instance of chromosomal fusion we observe can't be a new mutation
>rather than inheritance from parents.
no, John, I didn't and don't want to know why every instance of
chromosomal fusion we observe can't be a new mutation rather than
inheritance from parents.
I asked if it has been observed that two parents of different
chromosomal counts have produced offspring.
You offered karyotyping as a method of recognizing a change in
chromosome count in offspring.
I gave you a link that says that karyotyping can demonstrate that a
change in chromosome count in offspring has occurred during meiosis.
In other words, your offer of karyotyping as a means of determining
different chromosome count does not answer my question of whether
parents of different chromosome counts have produced viable offspring.
Since I've snipped the previous discussion that led up to this, I
guess the only way to verify this train of thought is to go back and
read the earlier posts.
> I told you that if we supposed
>this, any genetic study would be impossible. Hemophilia in the royal
>families of Europe is an example of such a study, one that would be
>impossible if we made your assumptions. Instead of tracing the disease
>back to Queen Victoria, we would just say that all the hemophiliacs were
>new mutants. Now, does that make sense? And forget the aneuploidy; it's
>a whole different phenomenon.
you just have not answered my question, that's all. Is this some new
tactic in which, I ask a question, you ignore the question, and
proceed to expound upon your evolutionary views, hoping to deflect
attention away from my question?
Zoe
>From: Zoe <muz...@aol.com>:
>
>> On Sat, 6 Aug 2005 00:13:48 -0400 (EDT), B Richardson
>> <br...@nym.hush.com> wrote:
>
><snipalot>
>
>> > Knowing how descent works is the only means
>> >that Harshman had at his disposal to identify the various
>> >members.
>
>> but I want to be told, how did John "know" how descent works?
>
>It has been studied by biologists for hundreds of years.
>In this case however I think that "how descent works" is
>more background knowledge, what specifically enabled him to
>solve the problem was his prior knowledge of the shape
>of the family tree of primates. The whole point was to
>demonstrate that any large enough section of DNA will produce
>the same tree.
the shape of the family tree is based on a subjective decision to use
certain objective traits for comparison rather than other objective
traits, and to use similarity as the standard for relationship.
No one has yet answered the question of why similarity automatically
means relationship. And if you say it doesn't automatically mean
relationship, then why is biological similarity the only exception to
the rule that says similarity does not necessarily mean relationship?
>
>> It is this initial "knowing", based on his faulty premise,
>
>What premise do you think is faulty?
the premise that says that similarity must automatically mean
relationship or common descent. There are too many exceptions to that
notion to make it a standard.
>
>> that is in question. So I'm not ready to move on to his findings
>> until he justifies his premise.
well, Eric? Do you want to take a shot at explaining why similarity
is a bona fide indicator of relationship?
snip>
>What on earth makes you think that computer languages _aren't_
>related by descent?
>
>If someone thinks they need a new programing language they
>in most cases won't make it up from scratch, rather they
>will look around for a language that is close to what they
>think they need and modify it.
there you go. You have identified how mental activity behaves, and
this very behavior can be recognized in the things of nature.
>See http://www.levenez.com/unix/history.html#06 for a small ;-)
>portion of the family tree of computer languages, variants of
>Unix and Linux.
you have addressed only Unix. I gave 145 different computer
languages. I would expect there to be relationship within the Unix
languages.
>Note that it is messier than, at least, the multicellular
>portion of the tree of life because the language developers
>sometimes combine features from two or more separate languages
>into their new language so that there are crosslinks where
>the branches come together again.
here, again, an example of how mental activity behaves.
>> And yet common
>> descent would not be a conclusion in this case.
>
>It most certainly would, at least within language families.
yes, within language families. I have no problem with the families.
I gave about 145 different families, though.
>
>> Here is a (copy and pasted) listing of 145 computer languages.
>> I'm betting that if you compare these, using similar programs as
>> used for genetic comparison, you will get patterns that could be
>> interpreted to mean relationship....except that there is no
>> common ancestor for all computer languages.
>
>It doesn't really matter whether there is a _single_ common
>ancestor for _all_ languages, if different language families
>have separate origins then we would end up with several
>separate trees, one for each separate group.
which is what can be done for biological entities -- several separate
trees, one for each separate group.
>But if everything comes together in a single consistant tree,
>like the tree of life, then that is very strong evidence for
>a single common origin.
there is no single consistent tree of life except the one drawn up
from the heads of onlookers. It is easy enough to draw a single
common ancestor on paper and start arbitrarily placing life forms
under them, based on similarities. The ability to do so doesn't make
it so in reality.
snip>
Zoe
<br...@nym.hush.com> wrote:
snip>
>>>The same thing could be done to identify various members
>>>of the human population where relation is documented by
>>>historical record using the *same* algorithm on the
>>>polymorphisms, the technique doesn't even work if there
>>>is no relation.
>>
>>can you provide some reference to your statement here?
>
>All kinds of pet projects are going on.
>
>http://freepages.genealogy.rootsweb.com/~allpoms/genetics1a.html
>
>I only looked at a couple. I liked this one:
>
>http://www.roperld.com/ycomparison.htm#37Markers
>
>He used the same tool I used in the second part of our
>excercise.
for starters, you do realize that these are tests done on the
Y-chromosomes of only members of the human family, not members of
families from different species.
Also, the following comment taken from your link is reminiscent of
what I read in Nature back in 2002. See sublink from the above link:
http://blairgenealogy.com/dna/dna101.html
"Mutations occur at random. This means IT IS POSSIBLE FOR TWO DISTANT
COUSINS TO MATCH EXACTLY ON ALL MARKERS WHILE TWO BROTHERS MIGHT NOT
MATCH EXACTLY. (Caps mine.) Because of the random nature of mutations
we must use statistics and probability to estimate the Time to the
Most Recent Common Ancestor (TMRCA). The actual calculations of TMRCA
are mathematically complex and depend on knowing the rate of mutation
and the true number of mutations. At this time there is not enough
data to accurately determine either of these factors so certain
assumptions have to be made. The discussion of these assumptions and
the actual calculations are beyond the scope of this webpage."
After reviewing your blairgenealogy link, I've come to the conclusion
that it is a lot of pseudo-scientific evo-speak directed at an effort
to validate the evolutionary concept of common descent. It is riddled
with false and faulty premises.
The section that I capitalized in the quote above corresponds with
what the article in Nature (or maybe it was Science) had said, that
people from one part of the world appeared to be genetically more
closely related than people or relatives from the same part of the
world. That, in itself, should disqualify the method of testing as
reliable for showing relationship. Instead, evolutionists press on,
insistent that mutations at STRs are meaningful with respect to
relationship.
To summarize: this is a lot of impressive-looking calculations, based
on false premises, thus making the calculations worthless. Frankly,
it is nonsense and a waste of time.
They need to justify their premises. They have not done so.
>> I remember
>>reading in Nature back in 2002, after the human genome sequencing was
>>completed, that it was found (using evolutionary principles of
>>relationship through DNA sequences) that humans from one part of the
>>world were more closely related to humans from another part of the
>>world, than they were to some of their own race or relatives. That,
>>alone, should disqualify the method as a means of establishing
>>relationship. I have looked for that particular issue of Nature, but
>>cannot lay my hands on it. Do you remember reading that article?
>>
>
>No.
too bad. It might have opened up your perspective a bit.
>>> Knowing how descent works is the only means
>>>that Harshman had at his disposal to identify the various
>>>members.
>>
>>but I want to be told, how did John "know" how descent works? It is
>>this initial "knowing", based on his faulty premise, that is in
>>question. So I'm not ready to move on to his findings until he
>>justifies his premise.
>>
>
>When things are copied and errors occur, the replicated copies
>inherit those errors. You find a unique fingerprint in the
>errors when all the descendants are examined.
similarity in errors do not necessarily mean relationship or common
descent. The same kinds of errors can occur simply because the
template is conducive to the same types of errors occurring.
A Corvette can break down because after, say, 50,000 miles, it needs
its timing belts changed. A Honda can also break down because after
50,000 miles, it needs its timing belts changed. Same problem,
different cars. That doesn't mean that the cars are related. They
just both have similarly designed engines that react to external
stimuli in the same way.
The same holds true for errors that occur repeatedly in different
situations. They may be found in varying situations, not because they
have been copied, but because the original design is susceptible to
similar environmental stimuli.
>The simplest way I can think of to explore this principle
>to take a simple text string of your choosing, make a
>couple of copies, introduce errors into the copies,
>make copies of the copies, and introduce errors into those
>copies and look over what you got. See if you can see
>anything in the inherited errors in a string that may
>indicate which string it was copied from, and which string
>its parent was copied from. You can make a branch by
>making two copies of a string and introducing different
>errors into their respective descendants.
this exercise would apply to known errors being passed down through
copying. It does not address the reality that similar designs can
suffer similar problems.
snip>
>>Here is a (copy and pasted) listing of 145 computer languages. I'm
>>betting that if you compare these, using similar programs as used for
>>genetic comparison, you will get patterns that could be interpreted to
>>mean relationship....except that there is no common ancestor for all
>>computer languages.
>>
>
>>From the group I have chosen Autolisp , Awk, csh, CSP, and Floop,
>and categorized them on a criterion.
>
>How would you match them up on the tree?:
>
> |-------A4
>|---+
>| |-------A5
>+
>| |---A2
>| |---+
>| | |---A3
>|---+
> |-------A1
>
>See what I mean? There's all sorts of meaningful ways to
>organize them, but subjective and not consistant. Without
>knowledge of the details I used to categorize them, the only
>ways to come up with the same tree as I did is by chance, or by
>selectively applying knowledge you have about those languages
>until you get the same tree.
I agree it is based on what traits are chosen to be used. All that
says is that it is a subjective choice of objective traits.
>Harshman identified which species
>the nucleotides I posted belonged to *without* using any
>detailed knowledge of the species themselves, and I concealed
>information about which was which.
again, I am not interested in if John can identify which species the
sequences came from. He needs to justify his premise that similarity
must means relationship and common descent. If there are exceptions
to the similarity standard (and there are many), then his premise is
fatally flawed.
>In part two of the excercise John
>didn't even have the nucleotides, I just created a tree using the
>nucleotides using the same tool that is being used at
>
>http://www.roperld.com/ycomparison.htm#37Markers
>
>That was also my first use of the tool, I'm a layperson
>like you and not a scientist like John or Steven J. So
>how were we able to pull this off?
by inputting the info into a program that has the database of these
species, there is no reason why the program should not spit back out
the correct I.D.s But that was not my question.
> We certainly can't do
>this with computer languages or sweaters without corroborating
>amongst ourselves.
corroboration had to occur for the program to be set up to recognize
the sequences. Those sequences weren't plugged into an empty program
and the identifications were made. There had to be a database
(corroborated by those who have studied the sequences) from which to
pull the matches.
In any event, that was not my question.
> What's more, if had accidently mixed up
>Colobus and Pongo and disputed Harshman's matchings, an examination
>of my files by a neutral third party would have shown the error
>to be mine.
again, I am not asking if you or John can identify the sequences. I
want justification for the premise that similarity must mean
relationship.
snip>
Harlequin
[snip]
> Also, the following comment taken from your link is reminiscent of
> what I read in Nature back in 2002. See sublink from the above link:
Zoe, why would you read _Nature_? You simply do not have the
background knowledge nor reading comprehension to deal anything
in that journal besides the trivial stuff like a news reports,
editorials, etc.
> http://blairgenealogy.com/dna/dna101.html
>
> "Mutations occur at random. This means IT IS POSSIBLE FOR TWO DISTANT
> COUSINS TO MATCH EXACTLY ON ALL MARKERS WHILE TWO BROTHERS MIGHT NOT
> MATCH EXACTLY. (Caps mine.) Because of the random nature of mutations
> we must use statistics and probability to estimate the Time to the
> Most Recent Common Ancestor (TMRCA). The actual calculations of TMRCA
> are mathematically complex and depend on knowing the rate of mutation
> and the true number of mutations. At this time there is not enough
> data to accurately determine either of these factors so certain
> assumptions have to be made. The discussion of these assumptions and
> the actual calculations are beyond the scope of this webpage."
>
> After reviewing your blairgenealogy link, I've come to the conclusion
> that it is a lot of pseudo-scientific evo-speak directed at an effort
> to validate the evolutionary concept of common descent. It is riddled
> with false and faulty premises.
There is ZERO "evo-speak" directed at an effort to "validate" common
descent. That would be a biological equivalent of trying to
validate that the Earth orbits the Sun in about a year's time.
Biologists simpley are not trying to validate common descent.
> The section that I capitalized in the quote above corresponds with
> what the article in Nature (or maybe it was Science) had said, that
> people from one part of the world appeared to be genetically more
> closely related than people or relatives from the same part of the
> world. That, in itself, should disqualify the method of testing as
> reliable for showing relationship. Instead, evolutionists press on,
> insistent that mutations at STRs are meaningful with respect to
> relationship.
No it is not. It is simply Zoe simply not understanding the material
yet again.
Let A have kids B and E. B has kids C and D. E has kids F and G:
C
B----|
| D
A---|
| F
E----|
G
If a mutation occurs in a particular marker for G and there is no
mutations in the others then for that marker F will resemble his
cousins C and D more than his brother G. Really basic stuff that
the geneticists all understand. If you only look at one marker
it is possible that this sort of thing will fool you. That is why
in a case like this one does not make such a determination based on
one marker. Now if one looked at enough distinct markers than one
can overcome this problem. One via math can put a probablity for each
particular hypothesis given some assumptions about mutation which
are testable in the real world.
The above is for the Y-chromosome which goes down male lines of
descent. For the non-sex chromosomes it becomes a bit more
complicated.
> To summarize: this is a lot of impressive-looking calculations, based
> on false premises, thus making the calculations worthless. Frankly,
> it is nonsense and a waste of time.
Please identify the false premise.
> They need to justify their premises. They have not done so.
False statement.
> >> I remember
> >>reading in Nature back in 2002, after the human genome sequencing was
> >>completed, that it was found (using evolutionary principles of
> >>relationship through DNA sequences) that humans from one part of the
> >>world were more closely related to humans from another part of the
> >>world, than they were to some of their own race or relatives. That,
> >>alone, should disqualify the method as a means of establishing
> >>relationship. I have looked for that particular issue of Nature, but
> >>cannot lay my hands on it. Do you remember reading that article?
> >>
> >
> >No.
>
> too bad. It might have opened up your perspective a bit.
It sounds like that you misremembered or more likely failed to
understand what was written. But in any event, no one here
is going to accept on your say so. Provide a citation.
> >>> Knowing how descent works is the only means
> >>>that Harshman had at his disposal to identify the various
> >>>members.
> >>
> >>but I want to be told, how did John "know" how descent works? It is
> >>this initial "knowing", based on his faulty premise, that is in
> >>question. So I'm not ready to move on to his findings until he
> >>justifies his premise.
> >>
> >
> >When things are copied and errors occur, the replicated copies
> >inherit those errors. You find a unique fingerprint in the
> >errors when all the descendants are examined.
>
> similarity in errors do not necessarily mean relationship or common
> descent. The same kinds of errors can occur simply because the
> template is conducive to the same types of errors occurring.
>
> A Corvette can break down because after, say, 50,000 miles, it needs
> its timing belts changed. A Honda can also break down because after
> 50,000 miles, it needs its timing belts changed. Same problem,
> different cars. That doesn't mean that the cars are related. They
> just both have similarly designed engines that react to external
> stimuli in the same way.
Your example is yet another example that you simply don't understand
what is going on. Mutations occur at random locations
in a genome. The possible number of mutations that can occur
is stagering. For point mutations it is in the billions. For
duplications
it far greater. Then there are reversals, inserting of foreign
material,
etc. The odds of two identical mutation occuring are very small.
The odds of two cars having problems with a belt is not. And besides
belt problems are not inherited.
> The same holds true for errors that occur repeatedly in different
> situations. They may be found in varying situations, not because they
> have been copied, but because the original design is susceptible to
> similar environmental stimuli.
This is false. The same mutation does NOT occur under similiar
enviromental
conditions and stimuli. Now there are circumstances that make it more
likely that a mutation will occur. And certainly some general classes
of mutation are more likley than others. But that is not we are
talking
about.
> >The simplest way I can think of to explore this principle
> >to take a simple text string of your choosing, make a
> >couple of copies, introduce errors into the copies,
> >make copies of the copies, and introduce errors into those
> >copies and look over what you got. See if you can see
> >anything in the inherited errors in a string that may
> >indicate which string it was copied from, and which string
> >its parent was copied from. You can make a branch by
> >making two copies of a string and introducing different
> >errors into their respective descendants.
>
> this exercise would apply to known errors being passed down through
> copying. It does not address the reality that similar designs can
> suffer similar problems.
Unclear on concept again. We are not talking about similiar mutations.
We are talking about identical mutations. That odds of these happening
even under nearly identical conditions is damn close to zero. We are
also talking about a pattern similiarity and disimiliarity which
is expected because of common descent. Manuscripts and living
things both show this sort of pattern while things not related by
common descent do not.
[snip]
> again, I am not interested in if John can identify which species the
> sequences came from. He needs to justify his premise that similarity
> must means relationship and common descent. If there are exceptions
> to the similarity standard (and there are many), then his premise is
> fatally flawed.
[snip]
Zoe, it has been repeately pointed out in this newsgroup that mere
similiarity is not the evidence for common descent.
It is the pattern of similiarity
and dissimiliarity. You are attacking a strawman.
--
Anti-spam: Replace "usenet" with "harlequin2"
B Richardson
>On Wed, 10 Aug 2005 15:11:30 -0400 (EDT), B Richardson
><br...@nym.hush.com> wrote:
>
>snip>
>
>>>>The same thing could be done to identify various members
>>>>of the human population where relation is documented by
>>>>historical record using the *same* algorithm on the
>>>>polymorphisms, the technique doesn't even work if there
>>>>is no relation.
>>>
>>>can you provide some reference to your statement here?
>>
>>All kinds of pet projects are going on.
>>
>>http://freepages.genealogy.rootsweb.com/~allpoms/genetics1a.html
>>
>>I only looked at a couple. I liked this one:
>>
>>http://www.roperld.com/ycomparison.htm#37Markers
>>
>>He used the same tool I used in the second part of our
>>excercise.
>
>for starters, you do realize that these are tests done on the
>Y-chromosomes of only members of the human family, not members of
>families from different species.
>
If you're asking, of course I know. That why I posted it, to satisfy
your request for a reference that human lineages documented
by historical record can be tracked with phylogenetic analysis.
>
>Also, the following comment taken from your link is reminiscent of
>what I read in Nature back in 2002. See sublink from the above link:
>
>http://blairgenealogy.com/dna/dna101.html
>
>"Mutations occur at random. This means IT IS POSSIBLE FOR TWO DISTANT
>COUSINS TO MATCH EXACTLY ON ALL MARKERS WHILE TWO BROTHERS MIGHT NOT
>MATCH EXACTLY. (Caps mine.)
And the brother that has picked up another marker not shared
by the other brother and distant cousin now can have a line
of descent traceable to uniquely him. These stray random
mutations are inherited, and if you have several of them
to work with you can build a phylogeny from them and trace lines
of descent back to where these random mutations occured
if you have enough data to work with.
Good point, but it rather supports phylogeny rather than
your criticism of it.
> Because of the random nature of mutations
>we must use statistics and probability to estimate the Time to the
>Most Recent Common Ancestor (TMRCA). The actual calculations of TMRCA
>are mathematically complex and depend on knowing the rate of mutation
>and the true number of mutations. At this time there is not enough
>data to accurately determine either of these factors so certain
>assumptions have to be made. The discussion of these assumptions and
>the actual calculations are beyond the scope of this webpage."
>
I'll not comment on TMRCA calculations, they are irrelevant
to this discussion.
>
>After reviewing your blairgenealogy link, I've come to the conclusion
>that it is a lot of pseudo-scientific evo-speak directed at an effort
>to validate the evolutionary concept of common descent. It is riddled
>with false and faulty premises.
>
I see nothing there about common descent, evolution, or
phylogeny. All I see is a few basic biology concepts.
Point out a faulty premise that you refer too.
>
>The section that I capitalized in the quote above corresponds with
>what the article in Nature (or maybe it was Science) had said, that
>people from one part of the world appeared to be genetically more
>closely related than people or relatives from the same part of the
>world. That, in itself, should disqualify the method of testing as
>reliable for showing relationship. Instead, evolutionists press on,
>insistent that mutations at STRs are meaningful with respect to
>relationship.
>
This is a little too vague to warrant muchcomment. You can go to their
site and register, then you can browse the abstracts. I suspect
crucial points are missing in your paraphrasing of the article's
focus.
>
>To summarize: this is a lot of impressive-looking calculations, based
>on false premises, thus making the calculations worthless. Frankly,
>it is nonsense and a waste of time.
>
Point out a calculation based on a false premise. Here's the
link again for convenience.
http://blairgenealogy.com/dna/dna101.html
>
>They need to justify their premises. They have not done so.
>
So state, for the record, the premise to which you are
referring. You use the word "premise" haphazardly on
different points, and in this case failed to point out
what it is you are referring to.
>
>>> I remember
>>>reading in Nature back in 2002, after the human genome sequencing was
>>>completed, that it was found (using evolutionary principles of
>>>relationship through DNA sequences) that humans from one part of the
>>>world were more closely related to humans from another part of the
>>>world, than they were to some of their own race or relatives. That,
>>>alone, should disqualify the method as a means of establishing
>>>relationship. I have looked for that particular issue of Nature, but
>>>cannot lay my hands on it. Do you remember reading that article?
>>>
>>
>>No.
>
>too bad. It might have opened up your perspective a bit.
>
I'm skeptical the article supports your criticism of phylogeny.
You claimed some items at the blairgeneology site supported
your criticims, they did not. I think my suspicion that a
vague reference to a Nature article that allegedly supports
your criticisms has been similarly muddled is warranted.
You can always produce a cite, you can browse abstracts free
of charge AFAIK.
>
>>>> Knowing how descent works is the only means
>>>>that Harshman had at his disposal to identify the various
>>>>members.
>>>
>>>but I want to be told, how did John "know" how descent works? It is
>>>this initial "knowing", based on his faulty premise, that is in
>>>question. So I'm not ready to move on to his findings until he
>>>justifies his premise.
>>>
>>
>>When things are copied and errors occur, the replicated copies
>>inherit those errors. You find a unique fingerprint in the
>>errors when all the descendants are examined.
>
>similarity in errors do not necessarily mean relationship or common
>descent. The same kinds of errors can occur simply because the
>template is conducive to the same types of errors occurring.
>
A few paragraphs earlier your criticism of phylogeny was the
randomness of mutations. Now you are claiming they occur
according to template?
Biases large enough to produce the phylogenies seen would
be easy to spot, why isn't anyone seeing them?
>
>A Corvette can break down because after, say, 50,000 miles, it needs
>its timing belts changed. A Honda can also break down because after
>50,000 miles, it needs its timing belts changed. Same problem,
>different cars. That doesn't mean that the cars are related. They
>just both have similarly designed engines that react to external
>stimuli in the same way.
>
Not relevant unless cars inherit errors.
>
>The same holds true for errors that occur repeatedly in different
>situations. They may be found in varying situations, not because they
>have been copied, but because the original design is susceptible to
>similar environmental stimuli.
>
Bias of the magnitude required to produce the phylogeny seen
would be easy to spot, it just isn't there.
>
>>The simplest way I can think of to explore this principle
>>to take a simple text string of your choosing, make a
>>couple of copies, introduce errors into the copies,
>>make copies of the copies, and introduce errors into those
>>copies and look over what you got. See if you can see
>>anything in the inherited errors in a string that may
>>indicate which string it was copied from, and which string
>>its parent was copied from. You can make a branch by
>>making two copies of a string and introducing different
>>errors into their respective descendants.
>
>this exercise would apply to known errors being passed down through
>copying. It does not address the reality that similar designs can
>suffer similar problems.
>
What your claiming just isn't seen on a scale large enough to
produce the same phylogeny for any gene, and would be impossible
to miss.
When John identified the species in the exercise, no traits were
used in the exercise, only nucleotides. No choice of traits was
done. I concealed the identity of the gene until after the identifications
were made, so any traits they may have caused were unknown.
>
>>Harshman identified which species
>>the nucleotides I posted belonged to *without* using any
>>detailed knowledge of the species themselves, and I concealed
>>information about which was which.
>
>again, I am not interested in if John can identify which species the
>sequences came from. He needs to justify his premise that similarity
>must means relationship and common descent. If there are exceptions
>to the similarity standard (and there are many), then his premise is
>fatally flawed.
>
Its not just similarity. I could have posted nucleotides
for only Pan and Pongo, similar species, he wouldn't
have been able to tell which was which without some detailed
knowledge of the nucleotides.
>
>>In part two of the excercise John
>>didn't even have the nucleotides, I just created a tree using the
>>nucleotides using the same tool that is being used at
>>
>>http://www.roperld.com/ycomparison.htm#37Markers
>>
>>That was also my first use of the tool, I'm a layperson
>>like you and not a scientist like John or Steven J. So
>>how were we able to pull this off?
>
>by inputting the info into a program that has the database of these
>species, there is no reason why the program should not spit back out
>the correct I.D.s But that was not my question.
>
No database was involved.
>
>> We certainly can't do
>>this with computer languages or sweaters without corroborating
>>amongst ourselves.
>
>corroboration had to occur for the program to be set up to recognize
>the sequences. Those sequences weren't plugged into an empty program
>and the identifications were made. There had to be a database
>(corroborated by those who have studied the sequences) from which to
>pull the matches.
>
No database, no corroboration, no wizard behind a curtain.
John could have done the same thing with pen and paper, its
tedious, the software is a labor saver. I could have
interchanged some of the ACTG symbols while retaining the
patterns of similarites and disimilarities and he still
could have done it.
>
>In any event, that was not my question.
>
>> What's more, if had accidently mixed up
>>Colobus and Pongo and disputed Harshman's matchings, an examination
>>of my files by a neutral third party would have shown the error
>>to be mine.
>
>again, I am not asking if you or John can identify the sequences. I
>want justification for the premise that similarity must mean
>relationship.
>
That you still think its purely similarity is indicative
that you simply don't understand phylogeny.
>snip>
>
>
>
John Harshman
That's where the tree comes in. As you recall, humans are more closely
related to chimps than chimps are to gorillas, gorillas are more closely
related to chimps and humans than to orangutans, etc. So there was no
common ancestor of gorillas, chimps, et cetera, unless et cetera
includes humans. And that's why three fissions would be needed if the
ancestor of the great apes had 23 chromosomes. One fission in the
ancestor of orangutans (after splitting from the human/chimp/gorilla
line), one in the ancestor of gorillas (after splitting from the
chimp/human line), and one in the ancestor of chimps (after splitting
from the human line).
> If you insist that the 24-chromosome population was more likely to
> start first, then you still have to explain how the first 24's
> differentiated into your hypothesized various species of apes. Your
> explanation for this differentiation could have taken place just as
> well before a fusion occurs, as after a fission occurs. It has
> nothing to do with parsimony.
Except that there was no such differentiation into "various species of
apes" unless you include humans in that group. This differentiation has
nothing to do with chromosome number, either. And it's not
"hypothesized"; the evidence is overwhelming.
> So I don't see how probability and statistics has an answer to
> something that you have no idea which came first, 23 or 24. How can
> odds be placed on an unknown?
It's not unknown. It's an unavoidable inference from the phylogenetic tree.
> It is not known if your "history" of
> ape chromosomes is even a reality. It's like saying, let's suppose
> that fairies exist and they have a human-like form. Now we can
> sequence DNA from humans and then we'll know what fairies' DNA was
> like.
No, it's nothing like that. We sequence DNA from actual organisms. That
tells us what their relationships are to each other. The chromosome
thing is a necessary consequence of those relationships. Conveniently,
the human chromosome in question shows the marks of fusion, in that it
has telomeres in the interior of the chromosome at just the spot they
would be expected, given a fusion.
> large snip of non-answers>
>
>>By the way, while I don't think it's important to this discussion,
>>"mutations are random" does *NOT* mean "all mutations are equally likely,"
>>or "all mutations are equally likely to be selected"
>
> isn't that the meaning of "random"? Why the specialized meaning of
> random in evolutionary theory then? Might as well use a different
> term.
No, it's just that you don't understand what "random" means. Not in
statistics or in biology. In statistics, "random" means that you can't
tell in advance what outcome you are going to get, like picking a number
out of a bag. But the bag doesn't have to have one each of every number.
It could have 10 ones, 5 twos and 1 three, for example. If you pick out
of this bag, you are very unlikely to pull a three as opposed to a one.
But the draw is still random. This is called a distribution. There can
be any distribution, and as long as the pick from that distribution is
not selecting a result based on anything other than its frequency in the
bag, the pick is random.
Now, in biology we have a restricted meaning with regard to mutation.
What "random" means in that context is merely that mutations do not
happen with regard to the current needs of the organism.
> snip>
>
>>>>also suspect that you have neither the intention nor the ability to tell
>>>>us
>>>>how "intelligence" (other, perhaps, than human intelligence) implements
>>>>any
>>>>"design" or change in design in living organisms.
>>>
>>>I cannot make a digestive system, so I cannot tell you how to do it.
>>>But if I were to try to recreate something that works like the
>>>digestive system, I certainly would not try to do it by random
>>>mutations. Would you? I would take note of the steps taken in a
>>>what-you-see-is-what-you-get system, and attempt to copy those, as far
>>>as possible. And that would be a useful, scientific venture, learning
>>>from nature, copying its processes, rather than speculating on its
>>>history.
>>>
>>
>>Why would you not use random mutations?
>
> would you? Observation of how mental activity behaves in the real
> world would tell you that things are not constructed through random
> activity. So if creation theory contends that the digestive system is
> not the result of random activity, this contention correlates well
> with how mental activity behaves.
People make use of randomness all the time, even in design. At the
simplest level, they sometimes flip a coin. And when you put a pot of
water on the stove to boil, you rely on the random collisions of atoms
to help make your tea. An evolutionary concept of God's creation is
similar to the latter: he sets up initial conditions -- big bang, first
cell, whatever -- such that known processes like random mutation and
natural selection will eventually produce the result he wants, while he
goes off to read a book until the pot boils.
>>If you don't know how to make a
>>digestive system, making lots of copies of an initial cell, varying them in
>>small ways, and seeing which ways move you closer to a digestive system,
>>might be a better idea than trying to dream up a complete digestive system
>
>>from scratch.
>
> trial and error is a tool of mental activity if a creator has not yet
> figured out how to make something. But unlike random mutations that
> have no idea that they want to make a digestive system, mental
> activity knows what it wants to make, and it plans and dreams and
> works towards its goal.
Sometimes it does, sometimes it doesn't. If people exhibit mental
activity, then they also certainly resort to trial and error quite
frequently.
>>Note that, before there are any digestive systems, you can't
>>very well copy one that already exists (since none do).
>
> my mention of copying had to do with how a creationist would approach
> science. They would copy nature, and learn how to use the principles
> seen in nature to create new things.
Why would this be different from the way anyone else would approach
science, or at least a small subset of science?
> But back before digestive systems existed on this earth, if you had to
> make a digestive system from scratch, I would hope you would put your
> mind to the task and figure out how best to approach it. You'd be
> fired on your first day on the job if you were caught sitting around
> idly doodling on your pad, hoping that something would come together
> on its own....which is the principle upon which evolutionary theory is
> based.
Would you consider all the animals with incomplete digestive systems to
be analogous to doodles? It seems to have taken life quite a while to
figure out that having distinct entrances and exits in the system would
be a good idea.
>>>>You have, in the consistent nested hierarchy of homologies,
>>>
>>>you have yet to demonstrate that nested hierarchies always mean common
>>>descent. If they do not always mean common descent, then on what
>>>basis do you decide that only the nested hierarchies of nature mean
>>>common descent?
>>>
>>
>>I have argued that *consistent* nested hierarchies -- seen if families of
>>hand-copied manuscripts, families of languages, and clades of living
>>organisms -- imply common descent. Your supposed counterexamples involve
>>sets of entities that fall into very different hierarchies depending on what
>>traits one chooses to examine and compare.
>
> there's the key: "Depending on what traits one chooses to examine and
> compare."
>
> Families of languages would not fall into a nested hierarchy if you
> chose other traits for comparison than the ones you have chosen to
> use. Those same languages that seem to fall into a nested hierarchy
> would not appear hierarchical if you chose to classify them according
> to other traits.
This is not actually true, if you're talking about natural languages.
They fall into a real, nested hierarchy. You would have to pick your
traits very carefully to avoid it. Or do you not believe that French and
Spanish are descended from Latin?
> Depending on the traits you choose to use for comparison you can get a
> nested hierarchy and even twin or triple-nested hierarchy, or none --
> all for the same groups.
I'd like to see you try. (I don't know what you mean here by "twin or
triple-nested", by the way.)
>>>>in biogeography,
>>>
>>>why does biogeography mean common descent, unless there is a
>>>preconceived notion in place?
>>>
>>
>>If, e.g. the various genera of the hominoids are not related, why do the two
>>living genera most genetically similar to humans share a continent with [a]
>>the greatest genetic diversity of humans (indicating humans have lived on
>>that continent longer than they've lived on other continenets), and [b] with
>>the australopiths, the extinct great ape genus most similar to our own genus
>>_Homo_.
>
> this, again, is the as-yet-unsupported premise that similarity means
> relationship. On what basis do you decide that similarity must means
> relationship for only biological life forms, but nowhere else? So
> far, this question has not been answered by anyone.
Yes it has, dozens of times. It's not the similarity per se. It's the
nested hierarchy.
>>>>in vestigial structures at the genetic and morphological level,
>>>
>>>the term "vestigial structures" is a term arising out of preconceived
>>>notions. Some may call the appendix vestigial, but there are uses for
>>>the appendix. Some may call the tailbone vestigial, but there are
>>>uses for the tailbone...and so on. To call something vestigial
>>>because it seems to have no use is a misunderstanding of and
>>>egotistical dismissal of structures that are really not vestigial at
>>>all.
>>>
>>
>>"Vestigial structures" are defined as having *reduced* function, not *no*
>>function, and can be recognized without regard to evolutionary notions.
>
> and what is the standard for reduced function? You have to first
> know the function of the supposed "vestige" in order to say its
> function has been reduced. It's too superficial to look at a
> similar-looking organ in another life form and decide that, therefore,
> this "vestigial" organ is indeed meant to function the same way as the
> other, but it's just not functioning anymore.
>
> You might as well look at the trunk of a car and call it vestigial
> because the tray of a pickup truck seems to perform a similar
> function, just more extensively.
If the trunk were reduced to the size of a glove compartment, we might
well call it vestigial. There is certainly a bit of subjectivity in how
reduced you need a function to be before you apply the term. Your main
idea, however, requires the denial of homology. You need to assume that
the coccyx has nothing to do at all with the tails of other vertebrates,
despite its detailed anatomical and developmental similarities, and that
nested hierarchy again.
>>Indeed, they can be recognized where evolution is rejected as an
>>explanation: the shortened simplified limbs of a thalidomide baby are
>>vestigial according to definition (that is, they lack some of the function
>>of homologous structures in related or allied organisms), but the vestigial
>>limbs aren't caused by any genetic change (the genes are unchanged), and
>>therefore cannot be an example of evolution. However, when vestigial
>>features are not the result of developmental derangement, it is reasonable
>>to ask why they share so many details of structure with organs with which
>>they do not share details of function, in species otherwise very similar to
>>the one with the vestigial structure.
>
> human creators use the same template for many different purposes. If
> mental activity is evidenced in the use of templates, why doesn't the
> similarity of structures not cause you to see mental activity here,
> also?
Two reasons. First, the nested hierarchy again. We just don't see nested
hierarchies being produced by human design. Second, humans use
functional templates. If your object needs to roll, you put wheels on
it. If it needs to fly, you don't take a wheel and bang it into shape to
be a wing; instead, you install a wing, a completely new structure for
the completely new function. That's just not what we see in the history
of life. We see old structures being turned to new and quite different
purposes.
>>Saying that the appendix is vestigial does not mean it does nothing; it
>>means that it occupies the location and shares embryological and anatomical
>>features with the caecum, a pouch used to digest leaves in many monkeys.
>
> no, no, no. The cecum or caecum in the monkey has its counterpart in
> the cecum or caecum of the human. Its counterpart is NOT the
> appendix. See:
>
> http://en.wikipedia.org/wiki/Caecum
>
> "Cecum or caecum is a pouch connected to the large intestine between
> the ileum and the colon. It is separated from the ileum by the
> ileocecal valve (ICV) or Bauhin's valve, and is considered to be the
> beginning of the large intestine and part of the colon.
>
> "Its primary function is to absorb water and salts from undigested
> food. It has a muscular wall that can knead the contents to enhance
> absorption.
>
> "The cecum is present in mammals, birds, and some reptiles."
You need to read a bit further. From the same source: "However, most
physicians and scientists believe the appendix lacks significant
function, and that it exists primarily as a vestigial remnant of the
larger cellulose-digesting cecum found in our herbivorous ancestors."
>>Since it doesn't digest leaves in humans, why does it have this location and
>>these traits?
>
> the appendix is not even designed to have supposedly digested leaves.
> It has a lymphatic function and seems well placed in an area that most
> needs it.
>
> See:
>
> http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Lymphoma?OpenDocument
>
> "The lymphatic system is part of the immune system, which defends the
> body against infection. It consists of lymph nodes connected by lymph
> vessels, which branch out into all parts of the body except the brain
> and spinal cord. The lymphatic system also includes the bone marrow,
> spleen, thymus gland, tonsils, adenoids and APPENDIX (caps mine.)"
>
> What better area to place an organ of the lymphatic system than at a
> point where bacteria are likely to be present?
You are picking and choosing little bits of your reference and ignoring
anything you don't like. That's called quote mining.
>> Why does the human tailbone, whatever its uses, share so many
>>homologies to actual tails in other primates (and other mammals)?
>
> based on how mental activity behaves, it is evident that a successful
> template works for many different purposes.
No it doesn't. A successful template works for the same purpose in many
contexts. Under the template theory, we would expect bird wings, bat
wins, and insect wings to all have the same structure. Instead, we find
that bird wings and theropod forelimbs have the same structure, rather
different from bat wings, and entirely unrelated to insect wings.
>> Vestigial
>>structures are simply an extreme case of the problem of "parahomology:"
>>similar designs for dissimilar functions. It's one thing to use commn
>>design for common purposes, but what logic (other than evolutionary logic,
>>in which the function of a structure can evolve over time, without erasing
>>all traces of the structure's history) is there to common design for
>>different purposes (especially when there is also -- consider bat, bird, and
>>pterosaur wings -- different design for common purposes).
>
> I suggest a study of how mental activity behaves when creating items,
> and you will get your answer as to common design for different
> purposes and different design for common purposes.
>
> Reducing this to basics, a rectangle is a common design used for many
> different purposes. Or a circle is a different design for common
> purposes.
Those are hardly designs at all. They're simple concepts at best. At any
rate, you seem to be making up the nature of mental activity to fit your
own template, and it doesn't seem to have anything to do either with
real mental activity or real living things.
> snip meanderings>
>
>>>>>A single cell exists, replicating itself repeatedly. Along comes a
>>>>>random "beneficial mutation." What happens next, based on your
>>>>>selection principle? How does the digestive system develop?
>>>>>
>>>>
>>>>It becomes a multicellular organism.
>>>
>>>could you be a little less vague? So you think that a single cell
>>>becoming multicellular is how a digestive system forms? Have you
>>>accounted for the changes in DNA sequences that are needed to produce
>>>the particular types of proteins needed to construct an esophagus, a
>>>stomach, duodenum, jejunum, small intestines, and all the attendant
>>>parts that make a digestive system work?
>>>
>>
>>Multicellularity preceeds specialization of the cells in question. For that
>>matter, formation of a digestive system preceeds all those specialized
>>subcomponents you mention.
>
> I'm afraid that formation of an overarching system to hold a digestive
> system precedes even the digestive system, not to mention the
> specialized subcomponents.
No idea what that meant. "Overarching system"?
> <snip inability to explain how selected mutations cause evolution>
You mean "snip your inability to understand what Steven is saying".
John Harshman
> John Harshman <jharshman....@pacbell.net> wrote:
>
> snip>
>
>>>>If a particular fusion is polymorphic within a population, surely it's
>>>>much more parsimonious to postulate a single fusion event than a new one
>>>>in each individual.
>>>
>>>
>>>so this postulation is not a result of observation but of speculation
>>>as to what is more parsimonious?
>>
>>It's hardly speculation. One event is more parsimonious than many.
>>That's what "parsimonious" means. If one event explains a set of
>>observations, we prefer that to many events.
>
> science is not about what is preferred but about what IS. In an area
> where the history is absent, the preference for parsimony does not
> produce evidence other than "it feels better this way."
Is it just vaguely possible that scientists understand the nature of
science a teeny bit better than you do? Your arrogance is amazing.
This is nothing more than applied probability. If you flip a coin 100
times and it comes up heads every time, are you justified in thinking
that it's not a regular coin, even without further examination?
Similarly, chromosomal fissions/fusions are not common events. If we can
explain the data by postulating just one of them rather than three or
more, we are justified in doing so. That's a normal scientific
inference. Get over it.
>>>>Why assume that Queen Victoria was the source
>>>>of hemophilia in the royal families of Europe? Couldn't every royal
>>>>hemophiliac have been a unique mutant?
>>>
>>>I think you've gotten away from karyotyping. Originally, you seemed
>>>to be saying that karyotyping would be the means of checking to see if
>>>two different-chromosome parents had bred.
>>
>>Yes. The karyotype of the offspring. Karyotypes are the basic data for
>>any study of chromosome numbers.
>>
>>
>>>At least that was the
>>>question I asked, and you answered with your karyotyping example. But
>>>according to the link I gave above, it says that cells end up with too
>>>many or too few chromosomes, not because parents had different
>>>chromosome counts, but because of problems with meiosis.
>>
>>And I told you that you the link was talking about aneuploidy, which has
>>nothing at all to do with chromosome fusion/fission, and thus nothing at
>>all to do with what we are talking about here.
>
> the link talks about karyotyping, which is what you offered as your
> evidence that two parents carried different chromosomes.
All karyotyping is is counting (and matching up) the chromosomes. That
has nothing to do with the question of why some cells have different
numbers of chromosomes from other cells. There are many ways this can
happen. One, the one the article is talking about, is aneuploidy.
Another is fission/fusion. The two are different, and what you say about
one does not apply to the other.
>>>So how did
>>>we get way over here in left field, inspecting poor dead Queen
>>>Victoria's chromosomes?
>>
>>Please wait while I count to 10 slowly. OK, back. You want to know why
>>every instance of chromosomal fusion we observe can't be a new mutation
>>rather than inheritance from parents.
>
> no, John, I didn't and don't want to know why every instance of
> chromosomal fusion we observe can't be a new mutation rather than
> inheritance from parents.
>
> I asked if it has been observed that two parents of different
> chromosomal counts have produced offspring.
>
> You offered karyotyping as a method of recognizing a change in
> chromosome count in offspring.
>
> I gave you a link that says that karyotyping can demonstrate that a
> change in chromosome count in offspring has occurred during meiosis.
>
> In other words, your offer of karyotyping as a means of determining
> different chromosome count does not answer my question of whether
> parents of different chromosome counts have produced viable offspring.
>
> Since I've snipped the previous discussion that led up to this, I
> guess the only way to verify this train of thought is to go back and
> read the earlier posts.
Never mind. The point is that aneuploidy and fission/fusion are
different. Aneuploidy is much more common. It's irrelevant to the
question. If you see identical fissions or fusions, it's much more
parsimonious (probability again) to suppose they are the result of a
single event than of multiple events. Not only are fissions/fusions
rare, but it's extremely unlikely that exactly the same one would happen
twice. So if you have individuals in a population that are homozygous
for the separate state, and individuals that are homozygous for the
fused state, and you come across an individual that's heterozygous, how
are *you* going to explain it? At any rate, there have in fact been
laboratory experiments in these populations, in which individuals of
different chromosome counts have been mated and have produced offspring.
>>I told you that if we supposed
>>this, any genetic study would be impossible. Hemophilia in the royal
>>families of Europe is an example of such a study, one that would be
>>impossible if we made your assumptions. Instead of tracing the disease
>>back to Queen Victoria, we would just say that all the hemophiliacs were
>>new mutants. Now, does that make sense? And forget the aneuploidy; it's
>>a whole different phenomenon.
>
> you just have not answered my question, that's all. Is this some new
> tactic in which, I ask a question, you ignore the question, and
> proceed to expound upon your evolutionary views, hoping to deflect
> attention away from my question?
No. You just don't understand the answers. I have tried to explain how
the answer is relevant to your question. I have failed.
Steven J.
are replying, is that orangutans differentiated from African apes *before*
African apes (including humans) differentiated from each other, and that
among African apes, gorillas differentiated from chimps/humans *before*
humans differentiated from chimps. This is based on comparisons of many,
many different DNA sequences and proteins, all of which show African apes
are more different from (and therefore, on the assumption of common descent,
split off from our family line before) orangutans than any of the African
apes are from each other, and most of which show that gorillas are more
different from humans and chimps than humans and chimps are from each other.
Never mind, just for the moment, that you don't accept such facts as
arguments for a literal tree of descent; just recall that evolutionists
accept them, and cannot suppose that one species (with 24 chromosome pairs)
could give rise to chimps, gorillas, and orangutatans without being
ancestral to humans (with 23 chromosome pairs) as well.
You are, by the way, correct to suppose that it was unlikely that the
chromosomal fusion would spread through the population and become fixed.
But then, there's no reason to suppose that the chromosomal fusion is
special, or beneficial, or important to anything (like erect posture, or
large brains, or whatnot) that make us human. It's just one of the neutral
mutations that happened to accumulate in the line leading up to us. Neutral
mutations are common, and some of them, by sheer chance, are going to become
fixed. Oddly, the ID proponent William Dembski makes a good point about
this: he warns us of the distinction between hitting a target with an arrow
("specification"), and drawing a target around wherever the arrow happened
to hit. The 23-chromosome-pair arrangement is just where, for us, the arrow
happened to hit.
>
> If you insist that the 24-chromosome population was more likely to
> start first, then you still have to explain how the first 24's
> differentiated into your hypothesized various species of apes. Your
> explanation for this differentiation could have taken place just as
> well before a fusion occurs, as after a fission occurs. It has
> nothing to do with parsimony.
>
You don't seem to understand my argument.
>
> So I don't see how probability and statistics has an answer to
> something that you have no idea which came first, 23 or 24. How can
> odds be placed on an unknown? It is not known if your "history" of
> ape chromosomes is even a reality. It's like saying, let's suppose
> that fairies exist and they have a human-like form. Now we can
> sequence DNA from humans and then we'll know what fairies' DNA was
> like.
>
First of all, it's not very much like that at all. We're hardly saying
"let's suppose chimpanzees and gorillas exist," or even "let's suppose
australopiths and ardipithecenes existed" (although we can directly examine
the genes of chimps and gorillas, which is not possible for extinct apes).
You seem quite obstinate in your refusal to learn anything or revise your
thinking here.
Second, as I've explained to you, there is no one-to-one mapping of genotype
onto phenotype, and no reason, in terms of genetics, for fairies to have
humanlike genomes simply because they have humanlike phenotypes.
>
> large snip of non-answers>
>
>>By the way, while I don't think it's important to this discussion,
>>"mutations are random" does *NOT* mean "all mutations are equally likely,"
>>or "all mutations are equally likely to be selected"
>
> isn't that the meaning of "random"? Why the specialized meaning of
> random in evolutionary theory then? Might as well use a different
> term.
>
John Harshman has already answered this (and your other points as well), but
let me try again. If I toss one six-sided die, I get a random result with
every possible outcome equally likely. But if I toss two six-sided dice, I
get a random outcome in which some outcomes (2 and 36) have only a 1 in 36
chance of happening, while another (7) has a 1 in 6 chance of occurring.
"Random" also has a common meaning of "unrelated to whatever purpose
something is needed for." If, e.g. I am on the streets and ask "random
strangers" for the time, that does not mean I am asking people who have no
reason to be on the street, or who might as well be in some other city, but
people who I have no particular reason to suppose know the correct time or
wish to tell me what it is.
>
> snip>
>
>>>>also suspect that you have neither the intention nor the ability to tell
>>>>us
>>>>how "intelligence" (other, perhaps, than human intelligence) implements
>>>>any
>>>>"design" or change in design in living organisms.
>>>
>>> I cannot make a digestive system, so I cannot tell you how to do it.
>>> But if I were to try to recreate something that works like the
>>> digestive system, I certainly would not try to do it by random
>>> mutations. Would you? I would take note of the steps taken in a
>>> what-you-see-is-what-you-get system, and attempt to copy those, as far
>>> as possible. And that would be a useful, scientific venture, learning
>>> from nature, copying its processes, rather than speculating on its
>>> history.
>>>
>>Why would you not use random mutations?
>
> would you? Observation of how mental activity behaves in the real
> world would tell you that things are not constructed through random
> activity. So if creation theory contends that the digestive system is
> not the result of random activity, this contention correlates well
> with how mental activity behaves.
>
In the real world, I note that genetic algorithms (attempts to
computer-model "Darwinian" evolution) are quite common design tools. So is
"brainstorming" -- sitting around and tossing out ideas more or less at
random. Later on, of course, one will have to go through these ideas, weed
some out and refine others -- but random activity is, in fact, a common
design tool.
>
>> If you don't know how to make a
>>digestive system, making lots of copies of an initial cell, varying them
>>in
>>small ways, and seeing which ways move you closer to a digestive system,
>>might be a better idea than trying to dream up a complete digestive system
>>from scratch.
>
> trial and error is a tool of mental activity if a creator has not yet
> figured out how to make something. But unlike random mutations that
> have no idea that they want to make a digestive system, mental
> activity knows what it wants to make, and it plans and dreams and
> works towards its goal.
>
>> Note that, before there are any digestive systems, you can't
>>very well copy one that already exists (since none do).
>
> my mention of copying had to do with how a creationist would approach
> science. They would copy nature, and learn how to use the principles
> seen in nature to create new things.
>
> But back before digestive systems existed on this earth, if you had to
> make a digestive system from scratch, I would hope you would put your
> mind to the task and figure out how best to approach it. You'd be
> fired on your first day on the job if you were caught sitting around
> idly doodling on your pad, hoping that something would come together
> on its own....which is the principle upon which evolutionary theory is
> based.
>
One hopes you are never put in charge of designing, well, anything,
anywhere, ever.
Of course, there's an interesting question here: why would the Intelligent
Designer of Life need to figure out how to put together a digestive system?
A problem with "intelligent design" as an explanation for biological
complexity was noted as far back as William Paley (1743 - 1805, the founder
of ID theory): an omnipotent designer doesn't *need* complicated systems
("contrivance," in Paley's term) to accomplish some goal. A Designer Who
can do anything can make a chunk of granite see, or digest food. Only a
designer constrained by the laws of physics and limited knowledge of the
universe has to "figure out" things and build complicated systems to
accomplish tasks.
>
> snip>
>
>>>>You have, in the consistent nested hierarchy of homologies,
>>>
>>> you have yet to demonstrate that nested hierarchies always mean common
>>> descent. If they do not always mean common descent, then on what
>>> basis do you decide that only the nested hierarchies of nature mean
>>> common descent?
>>>
>>I have argued that *consistent* nested hierarchies -- seen if families of
>>hand-copied manuscripts, families of languages, and clades of living
>>organisms -- imply common descent. Your supposed counterexamples involve
>>sets of entities that fall into very different hierarchies depending on
>>what
>>traits one chooses to examine and compare.
>
> there's the key: "Depending on what traits one chooses to examine and
> compare."
>
> Families of languages would not fall into a nested hierarchy if you
> chose other traits for comparison than the ones you have chosen to
> use. Those same languages that seem to fall into a nested hierarchy
> would not appear hierarchical if you chose to classify them according
> to other traits.
>
Can you give some examples here? To be sure, consistent nested hierarchies
are produced by branching descent with only "vertical" (from parent to
offspring) inheritance; one can mess up such nested hiearchies with
"lateral" transfer, and "lateral" transfer is common in languages. They can
borrow vocabulary, sounds, even grammatical features from each other. But
for all that, natural spoken languages (not to be confused with means of
*writing* those languages -- some languages have multiple writing systems)
fall into families nested in larger families, and the same pattern arises
when comparing many different sets of words, sounds, and grammar rules.
>
> Depending on the traits you choose to use for comparison you can get a
> nested hierarchy and even twin or triple-nested hierarchy, or none --
> all for the same groups.
>
Example, please?
>
>>>> in biogeography,
>>>
>>> why does biogeography mean common descent, unless there is a
>>> preconceived notion in place?
>>>
>>If, e.g. the various genera of the hominoids are not related, why do the
>>two
>>living genera most genetically similar to humans share a continent with
>>[a]
>>the greatest genetic diversity of humans (indicating humans have lived on
>>that continent longer than they've lived on other continenets), and [b]
>>with
>>the australopiths, the extinct great ape genus most similar to our own
>>genus
>>_Homo_.
>
> this, again, is the as-yet-unsupported premise that similarity means
> relationship. On what basis do you decide that similarity must means
> relationship for only biological life forms, but nowhere else? So
> far, this question has not been answered by anyone.
>
No, you don't seem to be paying any attention to my argument. I am not
*assuming* that humans are related to other African apes. I am noting that
we are, anatomically and genetically, more like chimps and gorillas than any
of us is like any other species, and anatomically, at least, the same goes
for the australopiths, and I'm asking, if these species all arose
separately, or if they all migrated from Noah's Ark, how did they all end up
in Africa together? Common descent (we are all in Africa because that's
where our last common ancestor lived) explains this. Separate creation
would make it rather unlikely that similar but separately created "kinds"
would end up close together (and close to fossils of similar, extinct
species) so often.
>
> snip>
>
>>>>in vestigial structures at the genetic and morphological level,
>>>
>>> the term "vestigial structures" is a term arising out of preconceived
>>> notions. Some may call the appendix vestigial, but there are uses for
>>> the appendix. Some may call the tailbone vestigial, but there are
>>> uses for the tailbone...and so on. To call something vestigial
>>> because it seems to have no use is a misunderstanding of and
>>> egotistical dismissal of structures that are really not vestigial at
>>> all.
>>>
>>"Vestigial structures" are defined as having *reduced* function, not *no*
>>function, and can be recognized without regard to evolutionary notions.
>
> and what is the standard for reduced function? You have to first
> know the function of the supposed "vestige" in order to say its
> function has been reduced. It's too superficial to look at a
> similar-looking organ in another life form and decide that, therefore,
> this "vestigial" organ is indeed meant to function the same way as the
> other, but it's just not functioning anymore.
>
So you are arguing that comparative anatomy is not possible?
"Carnivores, whose diet contains little or no plant material, have a reduced
caecum, often partially or wholly replaced by the vermiform appendix. The
appendix is a branch of the caecum."
I stand corrected, slightly. The caecum has its counterpart in the part of
the caecum that monkeys have, and we don't. You still have the question of
why we have this blockage- and infection-prone extension of the caecum,
instead of simply the smaller caecum (which could easily accomodate patches
of lymphatic tissue). A clearly example, I think, is the plantaris tendon;
it occurs in most (but not all) humans and all nonhuman apes. In nonhuman
apes it connects to the foot bones and enables the ape to clench its feet
into fists. In humans, its attachments are highly variable and it doesn't
help us move any part of our body. Again, this seems a moderately odd
feature, unless we inherited it (and lost part of its function, unless you
can grasp baseballs with your feet) from a common ancestor with nonhuman
apes.
>
> "Its primary function is to absorb water and salts from undigested
> food. It has a muscular wall that can knead the contents to enhance
> absorption.
>
> "The cecum is present in mammals, birds, and some reptiles."
>
>>Since it doesn't digest leaves in humans, why does it have this location
>>and
>>these traits?
>
> the appendix is not even designed to have supposedly digested leaves.
> It has a lymphatic function and seems well placed in an area that most
> needs it.
>
It's well placed, if its function were to digest leaves (for which,
admittedly, it does not seem well designed at all).
>
> See:
>
> http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Lymphoma?OpenDocument
>
> "The lymphatic system is part of the immune system, which defends the
> body against infection. It consists of lymph nodes connected by lymph
> vessels, which branch out into all parts of the body except the brain
> and spinal cord. The lymphatic system also includes the bone marrow,
> spleen, thymus gland, tonsils, adenoids and APPENDIX (caps mine.)"
>
> What better area to place an organ of the lymphatic system than at a
> point where bacteria are likely to be present?
>
Someplace where vagrant bits of undigested food can't block it off, and
start a fatal infection? Just a suggestion.
>
>> Why does the human tailbone, whatever its uses, share so many
>>homologies to actual tails in other primates (and other mammals)?
>
> based on how mental activity behaves, it is evident that a successful
> template works for many different purposes.
>
>> Vestigial
>>structures are simply an extreme case of the problem of "parahomology:"
>>similar designs for dissimilar functions. It's one thing to use commn
>>design for common purposes, but what logic (other than evolutionary logic,
>>in which the function of a structure can evolve over time, without erasing
>>all traces of the structure's history) is there to common design for
>>different purposes (especially when there is also -- consider bat, bird,
>>and
>>pterosaur wings -- different design for common purposes).
>
> I suggest a study of how mental activity behaves when creating items,
> and you will get your answer as to common design for different
> purposes and different design for common purposes.
>
I take this to be handwaving, rather than an answer.
>
> Reducing this to basics, a rectangle is a common design used for many
> different purposes. Or a circle is a different design for common
> purposes.
>
> snip meanderings>
>
>>>>> A single cell exists, replicating itself repeatedly. Along comes a
>>>>> random "beneficial mutation." What happens next, based on your
>>>>> selection principle? How does the digestive system develop?
>>>>>
>>>>It becomes a multicellular organism.
>>>
>>> could you be a little less vague? So you think that a single cell
>>> becoming multicellular is how a digestive system forms? Have you
>>> accounted for the changes in DNA sequences that are needed to produce
>>> the particular types of proteins needed to construct an esophagus, a
>>> stomach, duodenum, jejunum, small intestines, and all the attendant
>>> parts that make a digestive system work?
>>>
>>Multicellularity preceeds specialization of the cells in question. For
>>that
>>matter, formation of a digestive system preceeds all those specialized
>>subcomponents you mention.
>
> I'm afraid that formation of an overarching system to hold a digestive
> system precedes even the digestive system, not to mention the
> specialized subcomponents.
>
> <snip inability to explain how selected mutations cause evolution>
>
-- Steven J.
Don Cates
<sjt195...@nts.link.net.INVALID> wrote:
>
>"Zoe" <muz...@aol.com> wrote in message
>news:aj7tf1ddp8oc80isq...@4ax.com...
[snip]
>>
>> Depending on the traits you choose to use for comparison you can get a
>> nested hierarchy and even twin or triple-nested hierarchy, or none --
>> all for the same groups.
>>
>Example, please?
>>
Zoe doesn't understand what a 'twin nested hierarchy' is. She thinks
the 'twin' or 'triple' means 'two' or 'three'. Anyone can generate
several nested hierarchies for any rewasonable large collection of
entities, but they are almost certainly *not* 'twin' or 'multiple',
they are more like 'seventh cousins twice removed' hierarchies.
[snip]
--
Don Cates ("he's a cunning rascal" - PN)
Steven J.
"Don Cates" <catHO...@ms.umanitoba.ca> wrote in message
news:4300f7e6....@news.cc.umanitoba.ca...
entity could be part of multiple nested hiearchies that did not even contain
the same set of entities. There was also that discouraging moment when I
attempted to show that large differences in the genome could correspond to
trivial differences in phenotype (part of an argument that "98% sequence
similarity in DNA" does not have to mean "98% similarity in morphology and
behavior"), and she responded as though I'd been talking about the GULO
pseudogene. Sometimes arguing with Zoe feels like arguing with a
creationist redaction of the ELIZA program.
http://www.psych.utoronto.ca/~reingold/courses/ai/turing.html
>
> [snip]
> --
> Don Cates ("he's a cunning rascal" - PN)
>
-- Steven J.
Eric Rowley
> >From: Zoe <muz...@aol.com>: >
> >> On Sat, 6 Aug 2005 00:13:48 -0400 (EDT), B Richardson
> >> <br...@nym.hush.com> wrote: >
> ><snipalot>
> >
> >> > Knowing how descent works is the only means that
> >> > Harshman had at his disposal to identify the various
> >> >members.
> >> but I want to be told, how did John "know" how descent works?
> >It has been studied by biologists for hundreds of years. In
> >this case however I think that "how descent works" is more
> >background knowledge, what specifically enabled him to solve
> >the problem was his prior knowledge of the shape of the family
> >tree of primates. The whole point was to demonstrate that any
> >large enough section of DNA will produce the same tree.
> the shape of the family tree is based on a subjective decision
> to use certain objective traits for comparison rather than other
> objective traits,
No it isn't.
It's based on as many traits and as much DNA or Protein sequence
as possible and as John showed wih his two demonstrations
upthread, any long enough randomly chosen sequence of DNA will
tend to generate the same tree.
> and to use similarity as the standard for relationship.
Not similarity, a specific _pattern_ of similarities _and_
differences called a nested hierarchy.
(Is anybody keeping track of how many times Zoe has been told
this?)
<Snip further confusion between plain similarity and the
nested hierarchy.>
> >What on earth makes you think that computer languages _aren't_
> >related by descent?
> >If someone thinks they need a new programing language they in
> >most cases won't make it up from scratch, rather they will look
> >around for a language that is close to what they
> >think they need and modify it.
> there you go. You have identified how mental activity behaves,
> and this very behavior can be recognized in the things of
> nature.
Not really, one would expect more thinking ahead from mental
activity than we see in nature. Picking the best availablev
design for the job at hand for instance, rather than kludging
together something from whatever happens to be closest at hand.
> >See http://www.levenez.com/unix/history.html#06 for a small ;-)
> >portion of the family tree of computer languages, variants of
> >Unix and Linux.
> you have addressed only Unix. I gave 145 different computer
> languages. I would expect there to be relationship within the
> Unix languages.
And I would expect wide ranging relationships between languages
that appear rather dissimilar.
But this really is getting us nowhere since we don't know how
to put them into a tree and ,not knowing the actual relationships
for more than a few of them, we can't judge whether the
(hypothetical) tree shows real relationships or not.
> >Note that it is messier than, at least, the multicellular
> >portion of the tree of life because the language developers
> >sometimes combine features from two or more separate languages
> >into their new language so that there are crosslinks where
> >the branches come together again.
> here, again, an example of how mental activity behaves.
Note that this is an example of how the results of mental
activity differ from what is seen in nature.
> >> And yet common
> >> descent would not be a conclusion in this case.
> >It most certainly would, at least within language families.
> yes, within language families. I have no problem with the
> families. I gave about 145 different families, though.
No you didn't, I count 5 Basic's, 5 C's, 4 Lisp's, 2 Algol's
and 2 Pascal's.
And neither you nor I have any idea which of the other
languages are related to each other.
<snip>
> >It doesn't really matter whether there is a _single_ common
> >ancestor for _all_ languages, if different language families
> >have separate origins then we would end up with several
> >separate trees, one for each separate group.
> which is what can be done for biological entities --several
> separate trees, one for each separate group.
No, not unless you cheat.
> >But if everything comes together in a single consistant tree,
> >like the tree of life, then that is very strong evidence for
> >a single common origin.
> there is no single consistent tree of life except the one drawn
> up from the heads of onlookers.
Prove it!
Pick a sequence of a different gene than John used (for the same
species) and show how you get a different tree out of it.
> It is easy enough to draw a
> single common ancestor on paper and start arbitrarily placing
> life forms under them, based on similarities.
That isn't how it's done, reread Johns first demonstration
for a description of how it's done, from the other direction
and with no room for arbitrary decisions.
> The ability to do
> so doesn't make it so in reality.
Zoe, you're the only one shoehorning items into arbitrary
catagories and ignoring most of their properties to do so.
Accusing others of the same unscientific methods doesn't
make it so in reality.
Eric
Zoe
<sjt195...@nts.link.net.INVALID> wrote:
Steven, just so you know, I am not trying to be obstinate in my
responses to your posts. I truly come from a different world view and
have legitimate questions about yours. When I fail to agree with your
explanation, it is not because I see that you are right but refuse to
acknowledge it. It is because there are still questions in my mind
that haven't been answered persuasively. To me, there are other
reasonable and legitimate ways of viewing the data.
you got it coming and going, I see. Similarities mean relationship.
Dissimilarities mean relationship. And the unsupported premise for
"dissimilarity means relationship" is that differences must mean that
change has occurred over time, and the more change there is, the more
time must have passed. The conclusion based on this premise is that
degree of difference correlates with placement on a timeline.
Shouldn't the premise first be validated that differences between two
objects must invariably mean (1) that those differences are a result
of change in the original, and (2) that the more the difference, the
older the object?
Likewise, in the case of the similarity principle used for
relationship, shouldn't the premise first be validated that similarity
between two objects must invariably mean (1) that those similarities
are a result of relationship, and (2) that the more similar the
objects, the more closely related?
If there are numerous exceptions to the premise that
similarity/dissimilarity means relationship, then you don't have a
valid premise at all but just some made-up rules that fit a pet idea.
Anyway .... okay, so now we're talking about dissimilarities. If you
use the assumption that the more dissimilarities there are, the
further removed the relationship and therefore, the earlier in time,
then this undermines Richardson's blairgenealogy link that purports to
show relationship through mutations of the Y-chromosome.
Quote:
"It is possible for two distant cousins to match exactly on all
markers while two brothers might not match exactly."
End quote.
That would be saying, then, that one brother is further removed from
the common ancestor than the other one is, because there were
differences between them. Your principle of dissimilarity should be
consistent for all dissimilarities, otherwise it is not a principle at
all, but just a willy-nilly rule that is applied to whatever suits the
fancy.
>Never mind, just for the moment, that you don't accept such facts as
>arguments for a literal tree of descent; just recall that evolutionists
>accept them, and cannot suppose that one species (with 24 chromosome pairs)
>could give rise to chimps, gorillas, and orangutatans without being
>ancestral to humans (with 23 chromosome pairs) as well.
I do understand what evolutionists think about their trees. But you
haven't answered my question as to the validity of your premises.
You also have not answered why it is more likely that 24-chromosome
species would differentiate before fusion in one of its members, but
the same process of differentiation cannot occur after fission in one
of its members. And if the degree of difference between the 23's and
24's is the premise used to declare the 24's to be earlier, then you
need to validate that premise, that the more different the items, the
further back on a timeline one of them must have existed.
Can you validate these premises? If not, everything that follows
those premises, regardless of how technical and deeply reasoned, will
lead to a false conclusion, because your premise is false.
>You are, by the way, correct to suppose that it was unlikely that the
>chromosomal fusion would spread through the population and become fixed.
did I suppose this? I'm forgetting. I thought I had supposed that a
single 23-member with fission could be the ancestor of all
24-populations.
(Not that this is so critical, so I don't know why we're arguing it,
really.)
>But then, there's no reason to suppose that the chromosomal fusion is
>special, or beneficial, or important to anything (like erect posture, or
>large brains, or whatnot) that make us human. It's just one of the neutral
>mutations that happened to accumulate in the line leading up to us. Neutral
>mutations are common, and some of them, by sheer chance, are going to become
>fixed. Oddly, the ID proponent William Dembski makes a good point about
>this: he warns us of the distinction between hitting a target with an arrow
>("specification"), and drawing a target around wherever the arrow happened
>to hit. The 23-chromosome-pair arrangement is just where, for us, the arrow
>happened to hit.
so can you now validate the premises that I have listed above?
>> If you insist that the 24-chromosome population was more likely to
>> start first, then you still have to explain how the first 24's
>> differentiated into your hypothesized various species of apes. Your
>> explanation for this differentiation could have taken place just as
>> well before a fusion occurs, as after a fission occurs. It has
>> nothing to do with parsimony.
>>
>You don't seem to understand my argument.
I understand it very well. Can you validate your premises?
>> So I don't see how probability and statistics has an answer to
>> something that you have no idea which came first, 23 or 24. How can
>> odds be placed on an unknown? It is not known if your "history" of
>> ape chromosomes is even a reality. It's like saying, let's suppose
>> that fairies exist and they have a human-like form. Now we can
>> sequence DNA from humans and then we'll know what fairies' DNA was
>> like.
>>
>First of all, it's not very much like that at all. We're hardly saying
>"let's suppose chimpanzees and gorillas exist," or even "let's suppose
>australopiths and ardipithecenes existed" (although we can directly examine
>the genes of chimps and gorillas, which is not possible for extinct apes).
my point was not whether chimps and gorillas exist. My point is that
you don't know whether 23 or 24-chromosome populations existed first.
And until you validate your premise of differences meaning placement
on a timeline, the assumption of which came first is exactly the same
as an assumption that fairies exist. Neither can be demonstrated.
>You seem quite obstinate in your refusal to learn anything or revise your
>thinking here.
see my opening statement to this post.
>Second, as I've explained to you, there is no one-to-one mapping of genotype
>onto phenotype, and no reason, in terms of genetics, for fairies to have
>humanlike genomes simply because they have humanlike phenotypes.
since the mechanism of genetics is copying, there has to be a
one-to-one mapping of genotype to morphology. If the sequences are
the same, then the protein produced will be the same. If there are
slight variations so that the protein differs, I don't know how you
can even begin to say that similar sequences mean relationship. You
no longer have anything to work with. What looks like similar
sequences are really not producing similar results so even if chimp
DNA looks almost 99% similar, the fact is that those sequences are
producing different results, meaning they're really not similar after
all.
>> large snip of non-answers>
>>
>>>By the way, while I don't think it's important to this discussion,
>>>"mutations are random" does *NOT* mean "all mutations are equally likely,"
>>>or "all mutations are equally likely to be selected"
>>
>> isn't that the meaning of "random"? Why the specialized meaning of
>> random in evolutionary theory then? Might as well use a different
>> term.
>>
>John Harshman has already answered this (and your other points as well), but
>let me try again.
I do wish you would answer my questions directly. I asked why you
hsve a specialized meaning of random instead of the meaning given in
the regular dictionary. Why not use a different term to avoid
confusion?
> If I toss one six-sided die, I get a random result with
>every possible outcome equally likely. But if I toss two six-sided dice, I
>get a random outcome in which some outcomes (2 and 36) have only a 1 in 36
>chance of happening, while another (7) has a 1 in 6 chance of occurring.
when this happens, does the meaning of random change from "equally
likely to happen" to "less and less like to happen, depending on what
you're looking for"?
>"Random" also has a common meaning of "unrelated to whatever purpose
>something is needed for."
in short, random also has a common meaning of purposeless, right?
> If, e.g. I am on the streets and ask "random
>strangers" for the time, that does not mean I am asking people who have no
>reason to be on the street, or who might as well be in some other city, but
>people who I have no particular reason to suppose know the correct time or
>wish to tell me what it is.
the random choice for asking the time here is not purposeless. Your
purpose is to find out the time. The choice of who you ask may or may
not be random. It won't be random if you choose those people with
watches on their wrists. It would be random if you didn't look at
wrists but simply asked the time from the next person who happens
along. In the first case, your choices are not random. In the
second, you are equally likely to choose the person on your left as
the person on your right. I would call that random.
I did not say random activity is not part of design. I meant that you
do not construct anything by random activity alone. Evolutionary
theory claims that things are constructed by random activity alone.
It tries to insert selection as the non-intelligent answer for the
necessity of intelligence, but selection's choices themselves have to
be random since it is based on random activity.
snip>
>Of course, there's an interesting question here: why would the Intelligent
>Designer of Life need to figure out how to put together a digestive system?
how do you recommend that intelligence should behave, if not in
figuring out how to create something?
>A problem with "intelligent design" as an explanation for biological
>complexity was noted as far back as William Paley (1743 - 1805, the founder
>of ID theory): an omnipotent designer doesn't *need* complicated systems
>("contrivance," in Paley's term) to accomplish some goal. A Designer Who
>can do anything can make a chunk of granite see, or digest food. Only a
>designer constrained by the laws of physics and limited knowledge of the
>universe has to "figure out" things and build complicated systems to
>accomplish tasks.
if you set up laws by which you run your household, because you know
these laws are for the best good of your household, you still have to
figure out how to work within these laws in order to accomplish
certain goals. You might lay down the law that your children should
be in bed by 9:00 p.m. You also want to show them a fun DVD that is
three hours long. You work within the constraints of your own laws by
planning to start the showing at 6:00 p.m. so that your 9:00 p.m. law
will not be violated. Working within the confines of laws that you
have established because you know this is the best way to run your
household does not invalidate your "figurings."
On a more critical level, there are laws of the universe established
that cannot be broken (unlike the 9:00 p.m. ruling). These laws make
the universe what it is. To change them or break them would mean
changing the equilibrium of the universe. So in order to maintain
law, it must be figured out how to create within the boundaries of
these laws. In this way a designer is constrained by his own laws of
physics, not because of limited knowledge, but because of total
knowledge of what would happen if the laws were not operating as they
should.
And that is why God will not change His laws to save you. He had to
find another way to do so.
>> snip>
>>
>>>>>You have, in the consistent nested hierarchy of homologies,
>>>>
>>>> you have yet to demonstrate that nested hierarchies always mean common
>>>> descent. If they do not always mean common descent, then on what
>>>> basis do you decide that only the nested hierarchies of nature mean
>>>> common descent?
>>>>
>>>I have argued that *consistent* nested hierarchies -- seen if families of
>>>hand-copied manuscripts, families of languages, and clades of living
>>>organisms -- imply common descent. Your supposed counterexamples involve
>>>sets of entities that fall into very different hierarchies depending on
>>>what
>>>traits one chooses to examine and compare.
>>
>> there's the key: "Depending on what traits one chooses to examine and
>> compare."
>>
>> Families of languages would not fall into a nested hierarchy if you
>> chose other traits for comparison than the ones you have chosen to
>> use. Those same languages that seem to fall into a nested hierarchy
>> would not appear hierarchical if you chose to classify them according
>> to other traits.
>>
>Can you give some examples here?
you can choose to use traits such as geographical locations
(communities, ghettos) or types of literature, and those very same
languages will no longer fall into a nested hierarchy.
> To be sure, consistent nested hierarchies
>are produced by branching descent with only "vertical" (from parent to
>offspring) inheritance; one can mess up such nested hiearchies with
>"lateral" transfer, and "lateral" transfer is common in languages. They can
>borrow vocabulary, sounds, even grammatical features from each other. But
>for all that, natural spoken languages (not to be confused with means of
>*writing* those languages -- some languages have multiple writing systems)
>fall into families nested in larger families, and the same pattern arises
>when comparing many different sets of words, sounds, and grammar rules.
what traits are you using to construct the nested hierarchy?
>> Depending on the traits you choose to use for comparison you can get a
>> nested hierarchy and even twin or triple-nested hierarchy, or none --
>> all for the same groups.
>>
>Example, please?
let's take a hierarchy for all knitted products.
There is a common "language" running through all knitted items. The
pearl stitch and the knit stitch. Out of those two stitches come an
immense variety of patterns. The patterns can be arranged
hierarchically according to (1) use of the end product, (2) according
to patterns used, (3) according to materials used. Sweaters can be a
category in which uses might be for deep winter, fall weather, or just
plain clothing. Patterns can be categorized by, for instance,
cable-stitch patterns for adult sweaters; straight knitted stitches
for sweaters for babies. Materials would be heavier wools or cotton
for adults, or soft, fine wools for babies. A triple-nested hierarchy
can be developed for knitted items, using the traits of: use,
patterns, material. And all three traits would be found to be present
for all knitted items. Does this consistency mean relationship? Of
course not. They relate only in classification, not in the origins of
the knitted materials.
>>>>> in biogeography,
>>>>
>>>> why does biogeography mean common descent, unless there is a
>>>> preconceived notion in place?
>>>>
>>>If, e.g. the various genera of the hominoids are not related, why do the
>>>two
>>>living genera most genetically similar to humans share a continent with
>>>[a]
>>>the greatest genetic diversity of humans (indicating humans have lived on
>>>that continent longer than they've lived on other continenets), and [b]
>>>with
>>>the australopiths, the extinct great ape genus most similar to our own
>>>genus
>>>_Homo_.
>>
>> this, again, is the as-yet-unsupported premise that similarity means
>> relationship. On what basis do you decide that similarity must means
>> relationship for only biological life forms, but nowhere else? So
>> far, this question has not been answered by anyone.
>>
>No, you don't seem to be paying any attention to my argument. I am not
>*assuming* that humans are related to other African apes. I am noting that
>we are, anatomically and genetically, more like chimps and gorillas than any
>of us is like any other species,
isn't "more like" the same as similar? You are using similarity as a
basis for concluding relationship.
>and anatomically, at least, the same goes
>for the australopiths, and I'm asking, if these species all arose
>separately, or if they all migrated from Noah's Ark, how did they all end up
>in Africa together?
I don't have all the answers, and I don't want to get into the global
flood right now except to say that Mesopotamia, Sumeria, Africa, all
fit into the account of the starting over of life forms in this area
of the world called the cradle of civilization.
>Common descent (we are all in Africa because that's
>where our last common ancestor lived) explains this.
as does a starting over of life in this area explains it.
> Separate creation
>would make it rather unlikely that similar but separately created "kinds"
>would end up close together (and close to fossils of similar, extinct
>species) so often.
separate creation would not have taken place at the point where life
started over after a global flood. Common descent within species
would resume.
>> snip>
>>
>>>>>in vestigial structures at the genetic and morphological level,
>>>>
>>>> the term "vestigial structures" is a term arising out of preconceived
>>>> notions. Some may call the appendix vestigial, but there are uses for
>>>> the appendix. Some may call the tailbone vestigial, but there are
>>>> uses for the tailbone...and so on. To call something vestigial
>>>> because it seems to have no use is a misunderstanding of and
>>>> egotistical dismissal of structures that are really not vestigial at
>>>> all.
>>>>
>>>"Vestigial structures" are defined as having *reduced* function, not *no*
>>>function, and can be recognized without regard to evolutionary notions.
>>
>> and what is the standard for reduced function? You have to first
>> know the function of the supposed "vestige" in order to say its
>> function has been reduced. It's too superficial to look at a
>> similar-looking organ in another life form and decide that, therefore,
>> this "vestigial" organ is indeed meant to function the same way as the
>> other, but it's just not functioning anymore.
>>
>So you are arguing that comparative anatomy is not possible?
comparative anatomy for what purpose? For making up a historical past
for the life forms? Or for learning the functions and purposes of the
similarities and differences in order to further scientific research?
the first is useless speculation that contributes to nothing. The
second is science, pure and simple.
snip>
>>>Saying that the appendix is vestigial does not mean it does nothing; it
>>>means that it occupies the location and shares embryological and
>>>anatomical
>>>features with the caecum, a pouch used to digest leaves in many monkeys.
>>
>> no, no, no. The cecum or caecum in the monkey has its counterpart in
>> the cecum or caecum of the human. Its counterpart is NOT the
>> appendix. See:
>>
>> http://en.wikipedia.org/wiki/Caecum
>>
>> "Cecum or caecum is a pouch connected to the large intestine between
>> the ileum and the colon. It is separated from the ileum by the
>> ileocecal valve (ICV) or Bauhin's valve, and is considered to be the
>> beginning of the large intestine and part of the colon.
>>
>"Carnivores, whose diet contains little or no plant material, have a reduced
>caecum, often partially or wholly replaced by the vermiform appendix. The
>appendix is a branch of the caecum."
on what basis do you decide that the cecum has been replaced by the
appendix? It is not even listed as part of the lymphatic system. The
appendix, however, is part of the lymphatic system. And just because
the appendix is close to the cecum is not justification for deciding
that it is a branch of the cecum. The tongue is close to the gums.
Does that make the tongue a related branch of the gums? You arrest
here stating another premise that needs to be justified: That
proximity means relationship.
>I stand corrected, slightly. The caecum has its counterpart in the part of
>the caecum that monkeys have, and we don't. You still have the question of
>why we have this blockage- and infection-prone extension of the caecum,
>instead of simply the smaller caecum (which could easily accomodate patches
>of lymphatic tissue).
I don't tell nature how it should be. Nature should be studied for
what it is. What you see is what you get.
> A clearly example, I think, is the plantaris tendon;
>it occurs in most (but not all) humans and all nonhuman apes. In nonhuman
>apes it connects to the foot bones and enables the ape to clench its feet
>into fists. In humans, its attachments are highly variable and it doesn't
>help us move any part of our body. Again, this seems a moderately odd
>feature, unless we inherited it (and lost part of its function, unless you
>can grasp baseballs with your feet) from a common ancestor with nonhuman
>apes.
you seem to think that the only conclusion that can be drawn when
there are differences between species is that the function was lost.
Again, this seems to be a preconceived notion and a premise that has
no supporting evidence.
Please validate the premise that says that if there is a difference
between two things, it is because both things had the same function at
one time, but one lost the function.
>> "Its primary function is to absorb water and salts from undigested
>> food. It has a muscular wall that can knead the contents to enhance
>> absorption.
>>
>> "The cecum is present in mammals, birds, and some reptiles."
>>
>>>Since it doesn't digest leaves in humans, why does it have this location
>>>and
>>>these traits?
>>
>> the appendix is not even designed to have supposedly digested leaves.
>> It has a lymphatic function and seems well placed in an area that most
>> needs it.
>>
>It's well placed, if its function were to digest leaves (for which,
>admittedly, it does not seem well designed at all).
so why insist that its purpose must be to digest leaves, even when it
is obvious that it does not do so? It's like looking at a Corvette
that can go from 0 to 60 mph in two seconds, comparing it to a pickup
truck that takes 20 seconds to climb to 60, and saying that, clearly,
the pickup truck has lost the ability of the Corvette. Or it's like
saying that because the nose lies close to the top lip, the top lip
was meant to function like the nose, but has simply lost its ability
to breathe.
snip>
Zoe
<jharshman....@pacbell.net> wrote:
>Zoe wrote:
>
>> John Harshman <jharshman....@pacbell.net> wrote:
>>
>> snip>
>>
>>>>>If a particular fusion is polymorphic within a population, surely it's
>>>>>much more parsimonious to postulate a single fusion event than a new one
>>>>>in each individual.
>>>>
>>>>
>>>>so this postulation is not a result of observation but of speculation
>>>>as to what is more parsimonious?
>>>
>>>It's hardly speculation. One event is more parsimonious than many.
>>>That's what "parsimonious" means. If one event explains a set of
>>>observations, we prefer that to many events.
>>
>> science is not about what is preferred but about what IS. In an area
>> where the history is absent, the preference for parsimony does not
>> produce evidence other than "it feels better this way."
>
>Is it just vaguely possible that scientists understand the nature of
>science a teeny bit better than you do?
are you pulling rank on me, John? I can't help it if I have a mind in
my head and honest questions arise as to what some scientists think.
>Your arrogance is amazing.
if questioning your position is arrogance, then may arrogance prevail.
However, questioning a position is not evidence of arrogance, so you
have misjudged me.
>This is nothing more than applied probability. If you flip a coin 100
>times and it comes up heads every time, are you justified in thinking
>that it's not a regular coin, even without further examination?
what is in question is not whether it is a regular coin, but whether
it has been truly flipped 100 times in the past.
>Similarly, chromosomal fissions/fusions are not common events. If we can
>explain the data by postulating just one of them rather than three or
>more, we are justified in doing so. That's a normal scientific
>inference. Get over it.
sorry, authoritarianism is not going to work here. You have failed to
give persuasive answers, that's all there is to it, John.
>>>>>Why assume that Queen Victoria was the source
>>>>>of hemophilia in the royal families of Europe? Couldn't every royal
>>>>>hemophiliac have been a unique mutant?
>>>>
>>>>I think you've gotten away from karyotyping. Originally, you seemed
>>>>to be saying that karyotyping would be the means of checking to see if
>>>>two different-chromosome parents had bred.
>>>
>>>Yes. The karyotype of the offspring. Karyotypes are the basic data for
>>>any study of chromosome numbers.
>>>
>>>
>>>>At least that was the
>>>>question I asked, and you answered with your karyotyping example. But
>>>>according to the link I gave above, it says that cells end up with too
>>>>many or too few chromosomes, not because parents had different
>>>>chromosome counts, but because of problems with meiosis.
>>>
>>>And I told you that you the link was talking about aneuploidy, which has
>>>nothing at all to do with chromosome fusion/fission, and thus nothing at
>>>all to do with what we are talking about here.
>>
>> the link talks about karyotyping, which is what you offered as your
>> evidence that two parents carried different chromosomes.
>
>All karyotyping is is counting (and matching up) the chromosomes. That
>has nothing to do with the question of why some cells have different
>numbers of chromosomes from other cells.
and it has nothing to do with demonstrating that two parents of
different chromosomal counts were able to produce offspring. So why
did you offer it in answer to my question?
> There are many ways this can
>happen. One, the one the article is talking about, is aneuploidy.
>Another is fission/fusion. The two are different, and what you say about
>one does not apply to the other.
you still have not answered my question. Have studies been done that
demonstrate that parents of different chromosome counts have produced
viable offspring? To look at an offspring with a chromosome count
different from the parents does not answer this question. Change in
chromosome count has been observed to be a result of problems during
meiosis. What do you have to offer as evidence that parents of
different chromosome counts do indeed produce offspring with the new
chromosome count?
snip>
>No. You just don't understand the answers. I have tried to explain how
>the answer is relevant to your question. I have failed.
you certainly have failed, John, but not because I don't understand
your answers.
Repeat of a direct question: Have studies been done in which the
chromosome counts of parents were examined, found to be different, and
yet they produced viable offspring with a different chromosome count?
Zoe
snip>
>> there is no single consistent tree of life except the one drawn
>> up from the heads of onlookers.
>
>Prove it!
>
>Pick a sequence of a different gene than John used (for the same
>species) and show how you get a different tree out of it.
John didn't describe a tree. He simply identified which sequences
belonged to which species, based on a database of already discovered
sequences for the various species. I didn't ask him if he could
identify anything. I wanted him to validate his premises. So far, no
answer.
snip>
Zoe
>Zoe wrote:
>[snip]
>> Also, the following comment taken from your link is reminiscent of
>> what I read in Nature back in 2002. See sublink from the above link:
>
>
>Zoe, why would you read _Nature_? You simply do not have the
>background knowledge nor reading comprehension to deal anything
>in that journal besides the trivial stuff like a news reports,
>editorials, etc.
Question: Zoe, why don't you read the scientific journals instead of
spouting off the top of your head.
Comment: I read in Nature....."
Question: Zoe, why would you read Nature? You're simply not smart
enough to understand it.
can't win for losing, can I? :-\
>> http://blairgenealogy.com/dna/dna101.html
>>
>> "Mutations occur at random. This means IT IS POSSIBLE FOR TWO DISTANT
>> COUSINS TO MATCH EXACTLY ON ALL MARKERS WHILE TWO BROTHERS MIGHT NOT
>> MATCH EXACTLY. (Caps mine.) Because of the random nature of mutations
>> we must use statistics and probability to estimate the Time to the
>> Most Recent Common Ancestor (TMRCA). The actual calculations of TMRCA
>> are mathematically complex and depend on knowing the rate of mutation
>> and the true number of mutations. At this time there is not enough
>> data to accurately determine either of these factors so certain
>> assumptions have to be made. The discussion of these assumptions and
>> the actual calculations are beyond the scope of this webpage."
>>
>> After reviewing your blairgenealogy link, I've come to the conclusion
>> that it is a lot of pseudo-scientific evo-speak directed at an effort
>> to validate the evolutionary concept of common descent. It is riddled
>> with false and faulty premises.
>
>There is ZERO "evo-speak" directed at an effort to "validate" common
>descent. That would be a biological equivalent of trying to
>validate that the Earth orbits the Sun in about a year's time.
>Biologists simpley are not trying to validate common descent.
they have concluded, without grounds, that common descent from a
single common ancestor is a fact. Why should any thinking person
accept this assumption if it has not been validated?
>> The section that I capitalized in the quote above corresponds with
>> what the article in Nature (or maybe it was Science) had said, that
>> people from one part of the world appeared to be genetically more
>> closely related than people or relatives from the same part of the
>> world. That, in itself, should disqualify the method of testing as
>> reliable for showing relationship. Instead, evolutionists press on,
>> insistent that mutations at STRs are meaningful with respect to
>> relationship.
>
>No it is not. It is simply Zoe simply not understanding the material
>yet again.
>
>Let A have kids B and E. B has kids C and D. E has kids F and G:
>
> C
> B----|
> | D
> A---|
> | F
> E----|
> G
>
>
>If a mutation occurs in a particular marker for G and there is no
>mutations in the others then for that marker F will resemble his
>cousins C and D more than his brother G.
I'm hopeful that you are aware that the purpose of the Y-chromosome
study is to determine, via number of mutations, how close or distant
the person is from the common ancestor. Supposedly, the more
mutations (or changes or differences) the further removed is a member
from the common ancestor. Based on that assumption, then G, who is
the brother of F, will be further removed from the common ancestor
than is F.
Does that makes sense?
> Really basic stuff that the geneticists all understand. If you only look at one marker
>it is possible that this sort of thing will fool you. That is why
>in a case like this one does not make such a determination based on
>one marker. Now if one looked at enough distinct markers than one
>can overcome this problem. One via math can put a probablity for each
>particular hypothesis given some assumptions about mutation which
>are testable in the real world.
and what are these assumptions that are testable in the real world?
>The above is for the Y-chromosome which goes down male lines of
>descent. For the non-sex chromosomes it becomes a bit more
>complicated.
okay, let's just stay with the Y-chromosome then.
Please validate your hypothesis that number of markers in the
Y-chromosome is indicative of distance or closeness to some common
ancestor. What evidence do you have that says that number of
mutations means distance from LCA?
>> To summarize: this is a lot of impressive-looking calculations, based
>> on false premises, thus making the calculations worthless. Frankly,
>> it is nonsense and a waste of time.
>
>Please identify the false premise.
that changed markers in the Y-chromosome mean distance or closeness to
a common ancestor. On what grounds do you assert this?
snip>
>> >When things are copied and errors occur, the replicated copies
>> >inherit those errors. You find a unique fingerprint in the
>> >errors when all the descendants are examined.
>>
>> similarity in errors do not necessarily mean relationship or common
>> descent. The same kinds of errors can occur simply because the
>> template is conducive to the same types of errors occurring.
>>
>> A Corvette can break down because after, say, 50,000 miles, it needs
>> its timing belts changed. A Honda can also break down because after
>> 50,000 miles, it needs its timing belts changed. Same problem,
>> different cars. That doesn't mean that the cars are related. They
>> just both have similarly designed engines that react to external
>> stimuli in the same way.
>
>Your example is yet another example that you simply don't understand
>what is going on. Mutations occur at random locations
>in a genome. The possible number of mutations that can occur
>is stagering. For point mutations it is in the billions. For
>duplications
>it far greater. Then there are reversals, inserting of foreign
>material,
>etc. The odds of two identical mutation occuring are very small.
maybe so, IF you go down the road that the same changes are a result
of mutations. The same changes can be a result of the use of the same
template that reacts the same way to similar situations.
>The odds of two cars having problems with a belt is not. And besides
>belt problems are not inherited.
inheritance does not give you the clearance to stick whatever
unvalidated premises you like onto the biological life form. There
are too many exceptions to your assumptions to use inheritance as the
validation for your assumptions.
>> The same holds true for errors that occur repeatedly in different
>> situations. They may be found in varying situations, not because they
>> have been copied, but because the original design is susceptible to
>> similar environmental stimuli.
>
>This is false. The same mutation does NOT occur under similiar
>enviromental
>conditions and stimuli.
you are stuck on mutations. I am not saying that these are a result
of mutations but a result of similar templates responding in similar
manner to environmental stimuli.
> Now there are circumstances that make it more
>likely that a mutation will occur. And certainly some general classes
>of mutation are more likley than others. But that is not we are
>talking
>about.
right. We are not talking about mutations here, but about similar
templates.
>> >The simplest way I can think of to explore this principle
>> >to take a simple text string of your choosing, make a
>> >couple of copies, introduce errors into the copies,
>> >make copies of the copies, and introduce errors into those
>> >copies and look over what you got. See if you can see
>> >anything in the inherited errors in a string that may
>> >indicate which string it was copied from, and which string
>> >its parent was copied from. You can make a branch by
>> >making two copies of a string and introducing different
>> >errors into their respective descendants.
>>
>> this exercise would apply to known errors being passed down through
>> copying. It does not address the reality that similar designs can
>> suffer similar problems.
>
>Unclear on concept again. We are not talking about similiar mutations.
neither am I. Check back and see.
>We are talking about identical mutations.
you may be talking about identical mutations. I am talking about
identical templates.
snip>
>> again, I am not interested in if John can identify which species the
>> sequences came from. He needs to justify his premise that similarity
>> must means relationship and common descent. If there are exceptions
>> to the similarity standard (and there are many), then his premise is
>> fatally flawed.
>[snip]
>
>Zoe, it has been repeately pointed out in this newsgroup that mere
>similiarity is not the evidence for common descent.
>It is the pattern of similiarity
>and dissimiliarity. You are attacking a strawman.
neither similarity and dissimiliarity are sufficient to establish
common descent, not when there are thousands of exceptions to this
supposed rule.
Zoe
wrote:
snip>
zoe wrote:
>>Also, the following comment taken from your link is reminiscent of
>>what I read in Nature back in 2002. See sublink from the above link:
>>
>>http://blairgenealogy.com/dna/dna101.html
>>
>>"Mutations occur at random. This means IT IS POSSIBLE FOR TWO DISTANT
>>COUSINS TO MATCH EXACTLY ON ALL MARKERS WHILE TWO BROTHERS MIGHT NOT
>>MATCH EXACTLY. (Caps mine.)
>
>And the brother that has picked up another marker not shared
>by the other brother and distant cousin now can have a line
>of descent traceable to uniquely him.
this, to me, is nonsense. Just because one brother shows up with some
extra mutations does not mean that he alone is of a lineage further
removed or closer than that of his other brother. Son A and Son B
were both born of the same parents. Regardless of what changes there
are in the two sons, it does not make one son closer or further away
from his parents than the other. Many generations down the road,
offspring descended from Sons A and B will not have some members that
are closer or further from A and B's parents than their siblings.
So on what basis does the genealogist decide that one member is
further removed than another?
> These stray random
>mutations are inherited, and if you have several of them
>to work with you can build a phylogeny from them and trace lines
>of descent back to where these random mutations occured
>if you have enough data to work with.
anybody can do anything with any information. What needs to be
validated is the premises brought to the data.
snip>
>> Because of the random nature of mutations
>>we must use statistics and probability to estimate the Time to the
>>Most Recent Common Ancestor (TMRCA). The actual calculations of TMRCA
>>are mathematically complex and depend on knowing the rate of mutation
>>and the true number of mutations. At this time there is not enough
>>data to accurately determine either of these factors so certain
>>assumptions have to be made. The discussion of these assumptions and
>>the actual calculations are beyond the scope of this webpage."
>>
>
>I'll not comment on TMRCA calculations, they are irrelevant
>to this discussion.
in what way? This link was given supposedly to support the concept
that nested hierarchies and lineages can be traced via mutations. The
link does no such thing. The premise that time to the most recent
common ancestor can be calculated through mutations does nothing to
demonstrate a nested hierarchy, as far as I can see. Indeed, it
un-nests one brother from the other.
>>After reviewing your blairgenealogy link, I've come to the conclusion
>>that it is a lot of pseudo-scientific evo-speak directed at an effort
>>to validate the evolutionary concept of common descent. It is riddled
>>with false and faulty premises.
>>
>
>I see nothing there about common descent, evolution, or
>phylogeny. All I see is a few basic biology concepts.
"Time to the most recent common ancestor" surely speaks of common
descent and evolution over thousands of years, according to the
article.
>
>Point out a faulty premise that you refer too.
the faulty premise is that number of changes in the Y-chromosome must
mean distance or closeness to a common ancestor. On what basis?
snip>
> I suspect
>crucial points are missing in your paraphrasing of the article's
>focus.
>
>>
>>To summarize: this is a lot of impressive-looking calculations, based
>>on false premises, thus making the calculations worthless. Frankly,
>>it is nonsense and a waste of time.
>>
>
>Point out a calculation based on a false premise. Here's the
>link again for convenience.
>
>http://blairgenealogy.com/dna/dna101.html
The premise is that matched and mismatched markers are indicative of
closeness or distance from the most recent common ancestor. It is
assumed, without support, that the number of markers say something
about the distance from the LCA. On what basis?
Here's a section copied and pasted, since you asked for it:
Quote:
"Based on the above assumptions we derive the cumulative probability
table below. This table simply list the number of generations
corresponding to the 50%, 90% and 95% probability levels for various
numbers of matches.
Match
50%
90%
95%
95% Confidence Interval
12-0
Match exactly at all 12 markers
14
48
62
1-77
11-1
11 exact matches, 1 mismatch
37
85
103
5-121
10-2
10 exact matches, 2 mismatch
61
122
144
14-165
25-0
Match exactly at all 25 markers
7
23
30
0-37
24-1
24 exact matches, 1 mismatch
17
40
48
2-57
23-2
23 exact matches, 2 mismatch
28
56
66
6-75
"This table tells us that if we match on 24 of 25 markers there is a
50% probability that the most recent common ancestor is 17 generations
or less, a 90% probability that TMRCA is 40 generations or less, and a
95% probability that TMRCA is 48 generations or less. The 95%
Confidence Interval is the upper and lower range of values that
encompass 95% of the probability for the TMRCA. If we match on 24 of
25 markers, 95% of the possible TMRCA values fall between 2 and 57
generations."
End quote.
>>They need to justify their premises. They have not done so.
>>
>
>So state, for the record, the premise to which you are
>referring. You use the word "premise" haphazardly on
>different points, and in this case failed to point out
>what it is you are referring to.
I think that the faulty premise, in this instance, is that number of
markers must say something about distance from the last common
ancestor. And this premise is held so dearly that even when the
results are off the wall, with one brother being made to be closer to
the common ancestor than the other, no red flags are raised.
snip>
>>>When things are copied and errors occur, the replicated copies
>>>inherit those errors. You find a unique fingerprint in the
>>>errors when all the descendants are examined.
>>
>>similarity in errors do not necessarily mean relationship or common
>>descent. The same kinds of errors can occur simply because the
>>template is conducive to the same types of errors occurring.
>>
>
>A few paragraphs earlier your criticism of phylogeny was the
>randomness of mutations. Now you are claiming they occur
>according to template?
no, I am saying that the same templates can respond to the environment
in the same way. I am not saying that there are different templates
with mutations occurring in the same way to the different templates.
>Biases large enough to produce the phylogenies seen would
>be easy to spot, why isn't anyone seeing them?
who says no one is seeing them?
>>A Corvette can break down because after, say, 50,000 miles, it needs
>>its timing belts changed. A Honda can also break down because after
>>50,000 miles, it needs its timing belts changed. Same problem,
>>different cars. That doesn't mean that the cars are related. They
>>just both have similarly designed engines that react to external
>>stimuli in the same way.
>>
>
>Not relevant unless cars inherit errors.
okay, use computer programs then. Computer programs can inherit and
pass down viruses. Inheritance is not a sufficient reason to invoke
the faulty premises.
snip>
again, I did not ask if John could identify the species. I asked him
to defend his premise that similarity (and dissimilarity) invariably
means relationship and common descent. He has not done so.
>>>Harshman identified which species
>>>the nucleotides I posted belonged to *without* using any
>>>detailed knowledge of the species themselves, and I concealed
>>>information about which was which.
>>
>>again, I am not interested in if John can identify which species the
>>sequences came from. He needs to justify his premise that similarity
>>must means relationship and common descent. If there are exceptions
>>to the similarity standard (and there are many), then his premise is
>>fatally flawed.
>>
>
>Its not just similarity. I could have posted nucleotides
>for only Pan and Pongo, similar species, he wouldn't
>have been able to tell which was which without some detailed
>knowledge of the nucleotides.
you are still on the identification path. I am still on the
defense-of-premise path.
>>>In part two of the excercise John
>>>didn't even have the nucleotides, I just created a tree using the
>>>nucleotides using the same tool that is being used at
>>>
>>>http://www.roperld.com/ycomparison.htm#37Markers
>>>
>>>That was also my first use of the tool, I'm a layperson
>>>like you and not a scientist like John or Steven J. So
>>>how were we able to pull this off?
>>
>>by inputting the info into a program that has the database of these
>>species, there is no reason why the program should not spit back out
>>the correct I.D.s But that was not my question.
>>
>
>No database was involved.
really? I've never heard of a program without a database.
>>> We certainly can't do
>>>this with computer languages or sweaters without corroborating
>>>amongst ourselves.
>>
>>corroboration had to occur for the program to be set up to recognize
>>the sequences. Those sequences weren't plugged into an empty program
>>and the identifications were made. There had to be a database
>>(corroborated by those who have studied the sequences) from which to
>>pull the matches.
>>
>
>No database, no corroboration, no wizard behind a curtain.
>John could have done the same thing with pen and paper, its
>tedious, the software is a labor saver.
and doing it by pen and paper, what would have been his database to
work from, if not the already identified DNA sequences of the various
apes and human?
>I could have
>interchanged some of the ACTG symbols while retaining the
>patterns of similarites and disimilarities and he still
>could have done it.
done what? Identified which was which? Nice. But that was not what
I asked for. I asked for him to defend his premise that similarities
and dissimilarities invariably must mean relationship or common
descent.
snip>
Eric Rowley
> snip>
> >> there is no single consistent tree of life except the one
> >> drawn up from the heads of onlookers.
> >Prove it!
> >Pick a sequence of a different gene than John used (for the
> >same species) and show how you get a different tree out of it.
> John didn't describe a tree.
Yes he did.
Go back and reread the thread, you have totaly missunderstood
what John was doing.
:Neighbor-joining tree
:
:/------- SAMPLE A1
:| /--------------------------- SAMPLE A2
:.| /--+------------- SAMPLE A4
:\-+ /--------------------[...]-------------------
:SAMPLE A3
: \--------------+------------------------- SAMPLE A5
and
:One most parsimonious tree found:
:
:<pre>
:
: +----------------------B8
: +------------------6
: | | +---------------B7
: | +--------5
: | +-------------B6
: |
: 3--------------[off the page]------------------------------B4
: |
: | +----------------------B5
: +---------------4
: | +----------------B2
: +-----1
: | +---------B3
: +----------2
: +-----------B1
:
:</pre>
sure look like trees to me.
> He simply identified which sequences belonged to which species,
By using the sequences to calculate a tree (without knowing which
was which!) and comparing that tree to the accepted tree of
relationships.
> based on a database of already discovered sequences for the
> various species.
No, no, no!
The sequences come from a database of already discovered
sequences but then they were used without knowing which was which.
In his first demonstration on the 12th of april
http://www.talkorigins.org/origins/postmonth/apr05.html
(that wasn't in this thread but I think he reposted it here)
he picked the data himself but as he describes in the post
that knowledge isn't used.
In the second demonstration on the 4th of august
B Richardson posted the sequences without saying which was
which and John calculated the tree and used it to correctly
determine the species.
In the third, on the 8th of august B Richardson calculated
the tree and John matched it with the accepted tree of life.
So it was acctually only the second one that was done "blind"
but in the first one John shows exactly how he did it and the
program used in the second and third have no place to insert
the names of the species nor any database of sequences.
> I didn't ask him if he could identify anything. I wanted him to
> validate his premises. So far, no answer.
The fact that the nested hierarchy of life is real and
objective rather than arbitrary as you keep asserting goes a
long way towards validating the conclusion.
There certainly is no point in continuing until you understand
this.
Eric
John Harshman
I have difficulty interpreting this bit in the way Zoe wants, as an
honest disagreement. This is ridicule of Steven's position from a
position of ignorance, quite a different thing. I don't even think she
is seriously trying to understand him. Once more: it's the pattern of
similarities and differences among multiple species, the nested
hierarchy (is that phrase at all familiar?), the is the major evidence
for common descent. And it's the shape of the tree of common descent
that tells us that humans experienced a fusion, and that apes did not
experience fissions.
Now in the paragraph immediately above, Steve makes the assumption of a
molecular clock. He probably shouldn't have done this, and there's no
reason he needed to, because analyses that don't assume a clock will
give you the same tree anyway. But even with the clock assumption, it's
the combination of distances resulting in a nested hierarchly, and not
the distances themselves, that constitute evidence. The distances all
fit into a pattern, and that pattern is the same from gene to gene.
That's the evidence.
> Shouldn't the premise first be validated that differences between two
> objects must invariably mean (1) that those differences are a result
> of change in the original, and (2) that the more the difference, the
> older the object?
No, because that's not the premise. There is no such premise. No. Not.
> Likewise, in the case of the similarity principle used for
> relationship, shouldn't the premise first be validated that similarity
> between two objects must invariably mean (1) that those similarities
> are a result of relationship, and (2) that the more similar the
> objects, the more closely related?
That's not the premise either. Nested hierarchy nested hierarchy nested
hierarchy nested hierarchy nested hierarchy nested hieararchy.
[snip repetition of the same basic misunderstanding]
> You also have not answered why it is more likely that 24-chromosome
> species would differentiate before fusion in one of its members, but
> the same process of differentiation cannot occur after fission in one
> of its members. And if the degree of difference between the 23's and
> 24's is the premise used to declare the 24's to be earlier, then you
> need to validate that premise, that the more different the items, the
> further back on a timeline one of them must have existed.
None of this makes any sense. The reason for believing in fusion rather
than fission is like this:
1. We have a tree of relationships.
2. We have to put mutations on that tree so as to end up (in the
present) with the distribution of chromosome numbers we see, i.e. with
humans at N=23 and everyone else at N=24.
3. This can be done with one mutation if the ancestral state is 24 and
humans have the fusion.
4. It takes several mutations if the ancestral state is 23 and several
apes independently have a fission.
5. One fission can't account for it, because there is nowhere on the
tree you can put one fission and have the distribution of states
observed in living species.
[snip more repetition of the same misunderstanding]
>>Second, as I've explained to you, there is no one-to-one mapping of genotype
>>onto phenotype, and no reason, in terms of genetics, for fairies to have
>>humanlike genomes simply because they have humanlike phenotypes.
>
> since the mechanism of genetics is copying, there has to be a
> one-to-one mapping of genotype to morphology.
That made no sense, and I think it's because you don't know what Steven
means by "one-to-one" mapping.
> If the sequences are
> the same, then the protein produced will be the same.
True. But the point is that sequence differences do not always produce
morphological differences, and identical proteins can result in
different morphologies if non-coding, regulatory sequences change.
Further, since most DNA is junk, changes in that part of the DNA do not
produce any changes in phenotype. So you can have lots and lots of
molecular evolution accompanied by zero morphological evolution, or you
can have lots and lots of morphological evolution stemming from a teeny
amount of molecular evolution.
> If there are
> slight variations so that the protein differs, I don't know how you
> can even begin to say that similar sequences mean relationship. You
> no longer have anything to work with. What looks like similar
> sequences are really not producing similar results so even if chimp
> DNA looks almost 99% similar, the fact is that those sequences are
> producing different results, meaning they're really not similar after
> all.
This depends on what you mean by "similar". I would say that very
similar sequences can produce dissimilar results, but that doesn't
affect the fact that the sequences are similar. They don't just look
similar; they are similar. It only takes a few differences to make a big
change in morphology, as long as they're the right differences.
>>>large snip of non-answers>
>>>
>>>>By the way, while I don't think it's important to this discussion,
>>>>"mutations are random" does *NOT* mean "all mutations are equally likely,"
>>>>or "all mutations are equally likely to be selected"
>>>
>>>isn't that the meaning of "random"? Why the specialized meaning of
>>>random in evolutionary theory then? Might as well use a different
>>>term.
>>>
>>
>>John Harshman has already answered this (and your other points as well), but
>>let me try again.
>
> I do wish you would answer my questions directly. I asked why you
> hsve a specialized meaning of random instead of the meaning given in
> the regular dictionary. Why not use a different term to avoid
> confusion?
Many technical terms are not adequately explained in dictionaries. Get
used to it. I find this complaint ironic, by the way, coming from a
person who has a private definition for just about every term she uses.
>> If I toss one six-sided die, I get a random result with
>>every possible outcome equally likely. But if I toss two six-sided dice, I
>>get a random outcome in which some outcomes (2 and 36) have only a 1 in 36
>>chance of happening, while another (7) has a 1 in 6 chance of occurring.
>
> when this happens, does the meaning of random change from "equally
> likely to happen" to "less and less like to happen, depending on what
> you're looking for"?
No. The meaning of random is never "equally likely to happen", nor is it
ever "less and less likely to happen, depending on what you're looking for".
>>"Random" also has a common meaning of "unrelated to whatever purpose
>>something is needed for."
>
> in short, random also has a common meaning of purposeless, right?
That's a bit different, but sure, why not. You'll make some big deal out
of this having nothing to do with actual meanings, I imagine.
>>If, e.g. I am on the streets and ask "random
>>strangers" for the time, that does not mean I am asking people who have no
>>reason to be on the street, or who might as well be in some other city, but
>>people who I have no particular reason to suppose know the correct time or
>>wish to tell me what it is.
>
> the random choice for asking the time here is not purposeless. Your
> purpose is to find out the time. The choice of who you ask may or may
> not be random. It won't be random if you choose those people with
> watches on their wrists. It would be random if you didn't look at
> wrists but simply asked the time from the next person who happens
> along. In the first case, your choices are not random. In the
> second, you are equally likely to choose the person on your left as
> the person on your right. I would call that random.
Once again, you persist in taking irrelevant parts of analogies and
running off with them. All this was supposed to inform you of what
randomness means in genetics. Do you now understand that simple definition?
Sorry, that doesn't follow. Evolution has a random component, but it's
not entirely random. A football game has a random component too, the
opening coin toss. Is a football game therefore random? I think you are
trying to apply the law of contagion here, and that only works in magic.
> snip>
>
>>Of course, there's an interesting question here: why would the Intelligent
>>Designer of Life need to figure out how to put together a digestive system?
>
> how do you recommend that intelligence should behave, if not in
> figuring out how to create something?
If the intelligence is God, surely he doesn't have to figure anything
out. He can just declare it, and it happens. Omnipotence means never
having to say you're sorry -- I mean, never having to figure it out.
>>A problem with "intelligent design" as an explanation for biological
>>complexity was noted as far back as William Paley (1743 - 1805, the founder
>>of ID theory): an omnipotent designer doesn't *need* complicated systems
>>("contrivance," in Paley's term) to accomplish some goal. A Designer Who
>>can do anything can make a chunk of granite see, or digest food. Only a
>>designer constrained by the laws of physics and limited knowledge of the
>>universe has to "figure out" things and build complicated systems to
>>accomplish tasks.
>
> if you set up laws by which you run your household, because you know
> these laws are for the best good of your household, you still have to
> figure out how to work within these laws in order to accomplish
> certain goals. You might lay down the law that your children should
> be in bed by 9:00 p.m. You also want to show them a fun DVD that is
> three hours long. You work within the constraints of your own laws by
> planning to start the showing at 6:00 p.m. so that your 9:00 p.m. law
> will not be violated. Working within the confines of laws that you
> have established because you know this is the best way to run your
> household does not invalidate your "figurings."
Not if you're omnipotent. You could have a 3 hour show last only 3
seconds if you like. That's the thrill of omnipotence.
> On a more critical level, there are laws of the universe established
> that cannot be broken (unlike the 9:00 p.m. ruling). These laws make
> the universe what it is. To change them or break them would mean
> changing the equilibrium of the universe. So in order to maintain
> law, it must be figured out how to create within the boundaries of
> these laws. In this way a designer is constrained by his own laws of
> physics, not because of limited knowledge, but because of total
> knowledge of what would happen if the laws were not operating as they
> should.
He made them, he can break them. If he's constrained by the laws of
physics, what's all this about poofing species into existence?
> And that is why God will not change His laws to save you. He had to
> find another way to do so.
I refuse to argue theology with Zoe any further.
>>>>>>You have, in the consistent nested hierarchy of homologies,
>>>>>
>>>>>you have yet to demonstrate that nested hierarchies always mean common
>>>>>descent. If they do not always mean common descent, then on what
>>>>>basis do you decide that only the nested hierarchies of nature mean
>>>>>common descent?
>>>>>
>>>>
>>>>I have argued that *consistent* nested hierarchies -- seen if families of
>>>>hand-copied manuscripts, families of languages, and clades of living
>>>>organisms -- imply common descent. Your supposed counterexamples involve
>>>>sets of entities that fall into very different hierarchies depending on
>>>>what
>>>>traits one chooses to examine and compare.
>>>
>>>there's the key: "Depending on what traits one chooses to examine and
>>>compare."
>>>
>>>Families of languages would not fall into a nested hierarchy if you
>>>chose other traits for comparison than the ones you have chosen to
>>>use. Those same languages that seem to fall into a nested hierarchy
>>>would not appear hierarchical if you chose to classify them according
>>>to other traits.
>>>
>>
>>Can you give some examples here?
>
> you can choose to use traits such as geographical locations
> (communities, ghettos) or types of literature, and those very same
> languages will no longer fall into a nested hierarchy.
Those are not traits of the languages. Likewise, you could sort animals
alphabetically, and they wouldn't fit into a nested hierarchy. OK, we
agree that you can use really stupid traits that would destroy any
hierarchy. But there doesn't seem to be a point. We have reasons to
suppose that some traits should be useful and others should not, and we
can use the useful ones and ignore the useless ones. This shows nothing.
Do you agree, by the way, that languages actually are related by common
descent?
>> To be sure, consistent nested hierarchies
>>are produced by branching descent with only "vertical" (from parent to
>>offspring) inheritance; one can mess up such nested hiearchies with
>>"lateral" transfer, and "lateral" transfer is common in languages. They can
>>borrow vocabulary, sounds, even grammatical features from each other. But
>>for all that, natural spoken languages (not to be confused with means of
>>*writing* those languages -- some languages have multiple writing systems)
>>fall into families nested in larger families, and the same pattern arises
>>when comparing many different sets of words, sounds, and grammar rules.
>
> what traits are you using to construct the nested hierarchy?
Presence or absence of lexical and phonological features. For example,
languages that have a word for "father" that resembles "father", like
"pater", "foddir", "padre", etc. fall into one group. You can further
divide that into languages in which the word starts with f and those in
which it starts with p. Thus we separate out the Germanic languages from
the rest. And so on.
>>>Depending on the traits you choose to use for comparison you can get a
>>>nested hierarchy and even twin or triple-nested hierarchy, or none --
>>>all for the same groups.
>>>
>>
>>Example, please?
>
> let's take a hierarchy for all knitted products.
>
> There is a common "language" running through all knitted items. The
> pearl stitch and the knit stitch. Out of those two stitches come an
> immense variety of patterns. The patterns can be arranged
> hierarchically according to (1) use of the end product, (2) according
> to patterns used, (3) according to materials used. Sweaters can be a
> category in which uses might be for deep winter, fall weather, or just
> plain clothing. Patterns can be categorized by, for instance,
> cable-stitch patterns for adult sweaters; straight knitted stitches
> for sweaters for babies. Materials would be heavier wools or cotton
> for adults, or soft, fine wools for babies. A triple-nested hierarchy
> can be developed for knitted items, using the traits of: use,
> patterns, material. And all three traits would be found to be present
> for all knitted items. Does this consistency mean relationship? Of
> course not. They relate only in classification, not in the origins of
> the knitted materials.
Precisely. And because there is no single, natural hierarchy, because
the hierarchy is arbitrary, there is no reason to suppose that knitted
products have been produced through common descent. Contrast this to
life, in which there is indeed a single such hierarchy. Remember the
primates? You can't avoid the same hierarchy, whatever data you use. And
*that's* what we expect from common descent.
>>>>>>in biogeography,
>>>>>
>>>>>why does biogeography mean common descent, unless there is a
>>>>>preconceived notion in place?
>>>>>
>>>>
>>>>If, e.g. the various genera of the hominoids are not related, why do the
>>>>two
>>>>living genera most genetically similar to humans share a continent with
>>>>[a]
>>>>the greatest genetic diversity of humans (indicating humans have lived on
>>>>that continent longer than they've lived on other continenets), and [b]
>>>>with
>>>>the australopiths, the extinct great ape genus most similar to our own
>>>>genus
>>>>_Homo_.
>>>
>>>this, again, is the as-yet-unsupported premise that similarity means
>>>relationship. On what basis do you decide that similarity must means
>>>relationship for only biological life forms, but nowhere else? So
>>>far, this question has not been answered by anyone.
>>>
>>
>>No, you don't seem to be paying any attention to my argument. I am not
>>*assuming* that humans are related to other African apes. I am noting that
>>we are, anatomically and genetically, more like chimps and gorillas than any
>>of us is like any other species,
>
> isn't "more like" the same as similar? You are using similarity as a
> basis for concluding relationship.
No, he's noting the correspondence between similarity and geographic
proximity, and using that correspondence, not the similarity itself, as
evidence for relationship.
>>and anatomically, at least, the same goes
>>for the australopiths, and I'm asking, if these species all arose
>>separately, or if they all migrated from Noah's Ark, how did they all end up
>>in Africa together?
>
> I don't have all the answers, and I don't want to get into the global
> flood right now except to say that Mesopotamia, Sumeria, Africa, all
> fit into the account of the starting over of life forms in this area
> of the world called the cradle of civilization.
I don't want to get into it either, except to note that you just made no
sense at all. Of course we have no idea where in the geologic column you
think the flood lies, or if any or all of the various hominid fossils
come before or after it. But there seems to be no pattern of the sort
one might expect from your scenario, regardless.
>>Common descent (we are all in Africa because that's
>>where our last common ancestor lived) explains this.
>
>
> as does a starting over of life in this area explains it.
No it doesn't. We would expect the earliest hominid fossils to be found
in Mesopotamia if that were the case. Assuming those fossils are
post-flood. We would expect the earliest post-flood fossils of every
single "kind" to be in Mesopotamia, in fact. That expectation is not
borne out. Your flood is falsified once more.
>> Separate creation
>>would make it rather unlikely that similar but separately created "kinds"
>>would end up close together (and close to fossils of similar, extinct
>>species) so often.
>
> separate creation would not have taken place at the point where life
> started over after a global flood. Common descent within species
> would resume.
From the point where the ark landed, yes? So why aren't the earliest
fossils, or at least some fossils, of everything (literally) found in
Mesopotamia? Shouldn't there be hominids, aardvarks, Allosauruses,
kangaroos, Eryopses, chalicotheres, pronghorns, Smilodons, etc., all
within that little region?
>>>snip>
>>>
>>>>>>in vestigial structures at the genetic and morphological level,
>>>>>
>>>>>the term "vestigial structures" is a term arising out of preconceived
>>>>>notions. Some may call the appendix vestigial, but there are uses for
>>>>>the appendix. Some may call the tailbone vestigial, but there are
>>>>>uses for the tailbone...and so on. To call something vestigial
>>>>>because it seems to have no use is a misunderstanding of and
>>>>>egotistical dismissal of structures that are really not vestigial at
>>>>>all.
>>>>>
>>>>
>>>>"Vestigial structures" are defined as having *reduced* function, not *no*
>>>>function, and can be recognized without regard to evolutionary notions.
>>>
>>>and what is the standard for reduced function? You have to first
>>>know the function of the supposed "vestige" in order to say its
>>>function has been reduced. It's too superficial to look at a
>>>similar-looking organ in another life form and decide that, therefore,
>>>this "vestigial" organ is indeed meant to function the same way as the
>>>other, but it's just not functioning anymore.
>>>
>>
>>So you are arguing that comparative anatomy is not possible?
>
> comparative anatomy for what purpose? For making up a historical past
> for the life forms? Or for learning the functions and purposes of the
> similarities and differences in order to further scientific research?
> the first is useless speculation that contributes to nothing. The
> second is science, pure and simple.
And in fact comparative anatomy is quite useful in determining the
functions of previously unexamined structures. You don't have to dissect
a newly discovered species of mammal in order to know that it will have
a stomach. A newly discovered species of ruminant will have a four-part
stomach. And so on. Why should this be? Phylogeny makes sense of it.
>>>>Saying that the appendix is vestigial does not mean it does nothing; it
>>>>means that it occupies the location and shares embryological and
>>>>anatomical
>>>>features with the caecum, a pouch used to digest leaves in many monkeys.
>>>
>>>no, no, no. The cecum or caecum in the monkey has its counterpart in
>>>the cecum or caecum of the human. Its counterpart is NOT the
>>>appendix. See:
>>>
>>>http://en.wikipedia.org/wiki/Caecum
>>>
>>>"Cecum or caecum is a pouch connected to the large intestine between
>>>the ileum and the colon. It is separated from the ileum by the
>>>ileocecal valve (ICV) or Bauhin's valve, and is considered to be the
>>>beginning of the large intestine and part of the colon.
>>>
>>
>>"Carnivores, whose diet contains little or no plant material, have a reduced
>>caecum, often partially or wholly replaced by the vermiform appendix. The
>>appendix is a branch of the caecum."
>
> on what basis do you decide that the cecum has been replaced by the
> appendix? It is not even listed as part of the lymphatic system. The
> appendix, however, is part of the lymphatic system. And just because
> the appendix is close to the cecum is not justification for deciding
> that it is a branch of the cecum. The tongue is close to the gums.
> Does that make the tongue a related branch of the gums? You arrest
> here stating another premise that needs to be justified: That
> proximity means relationship.
The appendix is merely a reduced and constricted part of the caecum.
Proximity does mean relationship in a way. If some part in two organisms
is in the same location, with the same connections to other parts, we do
consider them homologous, even if the parts themselves are somewhat
different in shape. Usually, you do this without thinking about it. All
tetrapods (well, except snakes and such) have upper arm bones, and we
call those humeri. We call them the same bone even though their shapes
vary radically. Why? Because they are all attached to a shoulder girdle
at one end and two other bones, radius and ulna, at the other end. Same
with the appendix and caecum in different species.
>>I stand corrected, slightly. The caecum has its counterpart in the part of
>>the caecum that monkeys have, and we don't. You still have the question of
>>why we have this blockage- and infection-prone extension of the caecum,
>>instead of simply the smaller caecum (which could easily accomodate patches
>>of lymphatic tissue).
>
> I don't tell nature how it should be. Nature should be studied for
> what it is. What you see is what you get.
Precisely. And what you get is not basic designs for different purposes,
but adaptations of the same plan; thus we see vestigial organs.
>>A clearly example, I think, is the plantaris tendon;
>>it occurs in most (but not all) humans and all nonhuman apes. In nonhuman
>>apes it connects to the foot bones and enables the ape to clench its feet
>>into fists. In humans, its attachments are highly variable and it doesn't
>>help us move any part of our body. Again, this seems a moderately odd
>>feature, unless we inherited it (and lost part of its function, unless you
>>can grasp baseballs with your feet) from a common ancestor with nonhuman
>>apes.
>
> you seem to think that the only conclusion that can be drawn when
> there are differences between species is that the function was lost.
> Again, this seems to be a preconceived notion and a premise that has
> no supporting evidence.
>
> Please validate the premise that says that if there is a difference
> between two things, it is because both things had the same function at
> one time, but one lost the function.
Sure. It could instead be that god created a useless part that just
happened to resemble a useful part in some other animal. I see your point.
>>>"Its primary function is to absorb water and salts from undigested
>>>food. It has a muscular wall that can knead the contents to enhance
>>>absorption.
>>>
>>>"The cecum is present in mammals, birds, and some reptiles."
>>>
>>>
>>>>Since it doesn't digest leaves in humans, why does it have this location
>>>>and
>>>>these traits?
>>>
>>>the appendix is not even designed to have supposedly digested leaves.
>>>It has a lymphatic function and seems well placed in an area that most
>>>needs it.
>>>
>>
>>It's well placed, if its function were to digest leaves (for which,
>>admittedly, it does not seem well designed at all).
>
> so why insist that its purpose must be to digest leaves, even when it
> is obvious that it does not do so? It's like looking at a Corvette
> that can go from 0 to 60 mph in two seconds, comparing it to a pickup
> truck that takes 20 seconds to climb to 60, and saying that, clearly,
> the pickup truck has lost the ability of the Corvette. Or it's like
> saying that because the nose lies close to the top lip, the top lip
> was meant to function like the nose, but has simply lost its ability
> to breathe.
Sorry, those analogies were sense-free.
John Harshman
> On Sun, 14 Aug 2005 14:52:18 GMT, John Harshman
> <jharshman....@pacbell.net> wrote:
>
>
>>Zoe wrote:
>>
>>
>>>John Harshman <jharshman....@pacbell.net> wrote:
>>>
>>>snip>
>>>
>>>>>>If a particular fusion is polymorphic within a population, surely it's
>>>>>>much more parsimonious to postulate a single fusion event than a new one
>>>>>>in each individual.
>>>>>
>>>>>
>>>>>so this postulation is not a result of observation but of speculation
>>>>>as to what is more parsimonious?
>>>>
>>>>It's hardly speculation. One event is more parsimonious than many.
>>>>That's what "parsimonious" means. If one event explains a set of
>>>>observations, we prefer that to many events.
>>>
>>>science is not about what is preferred but about what IS. In an area
>>>where the history is absent, the preference for parsimony does not
>>>produce evidence other than "it feels better this way."
>>
>>Is it just vaguely possible that scientists understand the nature of
>>science a teeny bit better than you do?
>
>
> are you pulling rank on me, John? I can't help it if I have a mind in
> my head and honest questions arise as to what some scientists think.
No. I'm asking you to rein in your arrogance a bit and consider, just
for a moment, the possibility that you may not understand everything as
well as you imagine.
>
>>Your arrogance is amazing.
>
> if questioning your position is arrogance, then may arrogance prevail.
> However, questioning a position is not evidence of arrogance, so you
> have misjudged me.
It's not the questioning that's arrogant. It's the smug assurance that
scientists are idiots and that you have uncovered the basic flaws in all
our reasoning for the past hundred-plus years.
>>This is nothing more than applied probability. If you flip a coin 100
>>times and it comes up heads every time, are you justified in thinking
>>that it's not a regular coin, even without further examination?
>
> what is in question is not whether it is a regular coin, but whether
> it has been truly flipped 100 times in the past.
Again you persist in failing to see the point of the simplest analogies.
I don't know how to communicate with you.
>>Similarly, chromosomal fissions/fusions are not common events. If we can
>>explain the data by postulating just one of them rather than three or
>>more, we are justified in doing so. That's a normal scientific
>>inference. Get over it.
>
> sorry, authoritarianism is not going to work here. You have failed to
> give persuasive answers, that's all there is to it, John.
>
I don't think there is such a thing as a persuasive answer where you are
concerned. At this point I have to give up. I have explained this many
times, and you just don't read. I have no idea what's going on in your head.
>>>>>>Why assume that Queen Victoria was the source
>>>>>>of hemophilia in the royal families of Europe? Couldn't every royal
>>>>>>hemophiliac have been a unique mutant?
>>>>>
>>>>>I think you've gotten away from karyotyping. Originally, you seemed
>>>>>to be saying that karyotyping would be the means of checking to see if
>>>>>two different-chromosome parents had bred.
>>>>
>>>>Yes. The karyotype of the offspring. Karyotypes are the basic data for
>>>>any study of chromosome numbers.
>>>>
>>>>
>>>>
>>>>>At least that was the
>>>>>question I asked, and you answered with your karyotyping example. But
>>>>>according to the link I gave above, it says that cells end up with too
>>>>>many or too few chromosomes, not because parents had different
>>>>>chromosome counts, but because of problems with meiosis.
>>>>
>>>>And I told you that you the link was talking about aneuploidy, which has
>>>>nothing at all to do with chromosome fusion/fission, and thus nothing at
>>>>all to do with what we are talking about here.
>>>
>>>the link talks about karyotyping, which is what you offered as your
>>>evidence that two parents carried different chromosomes.
>>
>>All karyotyping is is counting (and matching up) the chromosomes. That
>>has nothing to do with the question of why some cells have different
>>numbers of chromosomes from other cells.
>
> and it has nothing to do with demonstrating that two parents of
> different chromosomal counts were able to produce offspring. So why
> did you offer it in answer to my question?
Karyotyping is a way to find out the chromosome count. The chromosome
count, in turn, can demonstrate that parents with different counts can
produce offspring. That's all.
>>There are many ways this can
>>happen. One, the one the article is talking about, is aneuploidy.
>>Another is fission/fusion. The two are different, and what you say about
>>one does not apply to the other.
>
> you still have not answered my question. Have studies been done that
> demonstrate that parents of different chromosome counts have produced
> viable offspring? To look at an offspring with a chromosome count
> different from the parents does not answer this question. Change in
> chromosome count has been observed to be a result of problems during
> meiosis. What do you have to offer as evidence that parents of
> different chromosome counts do indeed produce offspring with the new
> chromosome count?
One more time: the differences in chromosome counts you are talking
about are aneuploidy. You can't use aneuploidy as evidence for multiple
chromosomal fusion/fission events, just as you can't use the presence of
apples on a tree as evidence that you have an orange tree. Chromosome
fissions/fusions are very rare events. If you have a population with
variation in fissions/fusions, and you see many individuals who are
heterozygous for that fission/fusion, assuming that each of those
individuals is a separate mutation, happening in that generation, goes
against the laws of probability so much that we can ignore that idea.
>>No. You just don't understand the answers. I have tried to explain how
>>the answer is relevant to your question. I have failed.
>
> you certainly have failed, John, but not because I don't understand
> your answers.
How would you know, if you don't understand?
> Repeat of a direct question: Have studies been done in which the
> chromosome counts of parents were examined, found to be different, and
> yet they produced viable offspring with a different chromosome count?
>
I don't know. I'm too lazy to look it up. And it doesn't matter.
John Harshman
> On 13 Aug 2005 21:23:58 -0700, "Harlequin" <use...@cox.net> wrote:
>
>
>>Zoe wrote:
>>[snip]
>>
>>>Also, the following comment taken from your link is reminiscent of
>>>what I read in Nature back in 2002. See sublink from the above link:
>>
>>
>>Zoe, why would you read _Nature_? You simply do not have the
>>background knowledge nor reading comprehension to deal anything
>>in that journal besides the trivial stuff like a news reports,
>>editorials, etc.
>
>
> Question: Zoe, why don't you read the scientific journals instead of
> spouting off the top of your head.
Actually, the usual question is more like this:
Question: Zoe, why don't you read a basic textbook on biology so that
you can unlearn all the false notions you have developed, and will have
a chance of correctly interpreting some of the tidbits you pull off the web?
> Comment: I read in Nature....."
>
> Question: Zoe, why would you read Nature? You're simply not smart
> enough to understand it.
>
> can't win for losing, can I? :-\
Poor you.
>>>http://blairgenealogy.com/dna/dna101.html
>>>
>>>"Mutations occur at random. This means IT IS POSSIBLE FOR TWO DISTANT
>>>COUSINS TO MATCH EXACTLY ON ALL MARKERS WHILE TWO BROTHERS MIGHT NOT
>>>MATCH EXACTLY. (Caps mine.) Because of the random nature of mutations
>>>we must use statistics and probability to estimate the Time to the
>>>Most Recent Common Ancestor (TMRCA). The actual calculations of TMRCA
>>>are mathematically complex and depend on knowing the rate of mutation
>>>and the true number of mutations. At this time there is not enough
>>>data to accurately determine either of these factors so certain
>>>assumptions have to be made. The discussion of these assumptions and
>>>the actual calculations are beyond the scope of this webpage."
>>>
>>>After reviewing your blairgenealogy link, I've come to the conclusion
>>>that it is a lot of pseudo-scientific evo-speak directed at an effort
>>>to validate the evolutionary concept of common descent. It is riddled
>>>with false and faulty premises.
>>
>>There is ZERO "evo-speak" directed at an effort to "validate" common
>>descent. That would be a biological equivalent of trying to
>>validate that the Earth orbits the Sun in about a year's time.
>>Biologists simpley are not trying to validate common descent.
>
> they have concluded, without grounds, that common descent from a
> single common ancestor is a fact. Why should any thinking person
> accept this assumption if it has not been validated?
It has been validated. But that was a while ago. The earth orbiting the
sun was also validated quite some time ago. Scientists don't spend their
time trying to validate either of them today for exactly the same
reason. Old news; move along.
No, it makes no sense. Based on that assumption, G and F will be equally
far removed from the common ancestor. But this is only a statistical
statement. It doesn't mean that the number of mutations will be exactly
equal in all lineages, or that any small stretch of DNA will show such a
pattern. What it means is that, over a long period of time, about the
same number of mutations will accumulate in any long stretch of DNA in
different lineages. It won't apply over one generation, or at any one
site. You have a blind spot when it comes to statistics and
probabilities, so I'm pretty sure you won't understand this.
>>Really basic stuff that the geneticists all understand. If you only look at one marker
>>it is possible that this sort of thing will fool you. That is why
>>in a case like this one does not make such a determination based on
>>one marker. Now if one looked at enough distinct markers than one
>>can overcome this problem. One via math can put a probablity for each
>>particular hypothesis given some assumptions about mutation which
>>are testable in the real world.
>
> and what are these assumptions that are testable in the real world?
Independence of sites and the rates of particular mutation types.
>>The above is for the Y-chromosome which goes down male lines of
>>descent. For the non-sex chromosomes it becomes a bit more
>>complicated.
>
> okay, let's just stay with the Y-chromosome then.
>
> Please validate your hypothesis that number of markers in the
> Y-chromosome is indicative of distance or closeness to some common
> ancestor. What evidence do you have that says that number of
> mutations means distance from LCA?
That's how mutation works. It's a random thing. One happens every so
often, and they pile up. If you assay a large enough number of sites the
randomness averages out. It's just like coin flipping. If I flip a coin
once, nobody can say whether it will be heads or tails. If I flip a coin
100,000 times, we can say that very close to 50% of the total will be heads.
>>>To summarize: this is a lot of impressive-looking calculations, based
>>>on false premises, thus making the calculations worthless. Frankly,
>>>it is nonsense and a waste of time.
>>
>>Please identify the false premise.
>
> that changed markers in the Y-chromosome mean distance or closeness to
> a common ancestor. On what grounds do you assert this?
If it's a false premise, that means that changed markers don't mean
closeness to a common ancestor. On what grounds do ou assert this? Or
did you mean "unproven premise" instead of "false premise"?
What this is based on is the observed randomness of mutations. That's
really all you need.
>>>>When things are copied and errors occur, the replicated copies
>>>>inherit those errors. You find a unique fingerprint in the
>>>>errors when all the descendants are examined.
>>>
>>>similarity in errors do not necessarily mean relationship or common
>>>descent. The same kinds of errors can occur simply because the
>>>template is conducive to the same types of errors occurring.
>>>
>>>A Corvette can break down because after, say, 50,000 miles, it needs
>>>its timing belts changed. A Honda can also break down because after
>>>50,000 miles, it needs its timing belts changed. Same problem,
>>>different cars. That doesn't mean that the cars are related. They
>>>just both have similarly designed engines that react to external
>>>stimuli in the same way.
>>
>>Your example is yet another example that you simply don't understand
>>what is going on. Mutations occur at random locations
>>in a genome. The possible number of mutations that can occur
>>is stagering. For point mutations it is in the billions. For
>>duplications
>>it far greater. Then there are reversals, inserting of foreign
>>material,
>>etc. The odds of two identical mutation occuring are very small.
>
> maybe so, IF you go down the road that the same changes are a result
> of mutations. The same changes can be a result of the use of the same
> template that reacts the same way to similar situations.
That made no sense at all. Perhaps you could explain in more detail,
with more reference to real biology. What template?
>>The odds of two cars having problems with a belt is not. And besides
>>belt problems are not inherited.
>
> inheritance does not give you the clearance to stick whatever
> unvalidated premises you like onto the biological life form. There
> are too many exceptions to your assumptions to use inheritance as the
> validation for your assumptions.
Explain. What exceptions?
>>>The same holds true for errors that occur repeatedly in different
>>>situations. They may be found in varying situations, not because they
>>>have been copied, but because the original design is susceptible to
>>>similar environmental stimuli.
>>
>>This is false. The same mutation does NOT occur under similiar
>>enviromental
>>conditions and stimuli.
>
> you are stuck on mutations. I am not saying that these are a result
> of mutations but a result of similar templates responding in similar
> manner to environmental stimuli.
What template? And are we using some new definition of mutation such
that changes in DNA are not mutations?
[snip more repetition about this mysterious "template"]
>>>again, I am not interested in if John can identify which species the
>>>sequences came from. He needs to justify his premise that similarity
>>>must means relationship and common descent. If there are exceptions
>>>to the similarity standard (and there are many), then his premise is
>>>fatally flawed.
>>
>>[snip]
>>
>>Zoe, it has been repeately pointed out in this newsgroup that mere
>>similiarity is not the evidence for common descent.
>>It is the pattern of similiarity
>>and dissimiliarity. You are attacking a strawman.
>
> neither similarity and dissimiliarity are sufficient to establish
> common descent, not when there are thousands of exceptions to this
> supposed rule.
What exceptions are you talking about, exactly? And you missed the
relevant word: pattern. By which he means nested hierarchy. Remember
that? Here:
1. It has been shown to you that life, particularly, here, DNA sequences
in primates, display nested hierarchy.
2. It has been shown to you that this hierarchy is consistent and
non-arbitrary.
3. It has been shown to you that sweaters, for example, display no such
consistent, non-arbitrary hierarchy.
4. It has been shown to you that such a hierarchy is to be expected from
common descent with branching, and from no other known process.
You consistently refuse to hold all this in your head at one time. You
keep going back to your notions of "similarity proves relationship" and
other such strawmen and misconceptions. I'm asking you to please try to
remember these simple facts and not to go back to your strawmen.
John Harshman
> On Sun, 14 Aug 2005 03:57:30 EDT, B Richardson <br...@nym.hush.com>
> wrote:
>
> snip>
>
> zoe wrote:
>
>
>>>Also, the following comment taken from your link is reminiscent of
>>>what I read in Nature back in 2002. See sublink from the above link:
>>>
>>>http://blairgenealogy.com/dna/dna101.html
>>>
>>>"Mutations occur at random. This means IT IS POSSIBLE FOR TWO DISTANT
>>>COUSINS TO MATCH EXACTLY ON ALL MARKERS WHILE TWO BROTHERS MIGHT NOT
>>>MATCH EXACTLY. (Caps mine.)
>>
>>And the brother that has picked up another marker not shared
>>by the other brother and distant cousin now can have a line
>>of descent traceable to uniquely him.
>
>
> this, to me, is nonsense. Just because one brother shows up with some
> extra mutations does not mean that he alone is of a lineage further
> removed or closer than that of his other brother.
Further removed or closer to what? All he's saying is that the
descendants of this brother can, in the future, be distinguished from
descendants of the other brother, and everyone else, by possession of
this new marker.
> Son A and Son B
> were both born of the same parents. Regardless of what changes there
> are in the two sons, it does not make one son closer or further away
> from his parents than the other. Many generations down the road,
> offspring descended from Sons A and B will not have some members that
> are closer or further from A and B's parents than their siblings.
>
> So on what basis does the genealogist decide that one member is
> further removed than another?
Further removed is perhaps the wrong word and has confused you. If two
people share a particular marker, it suggests that they are more closely
related, i.e. they share a more recent common ancestor, than they share
with anyone who lacks the marker. Just like the brother's mutation is
passed on to his descendants and marks them as related through him, and
thus more closely related to him than to the other brother. Again, this
is a statistical judgment. Identical mutations can indeed happen twice,
and recombination means that there are no pure lineages anyway. But if
you look at enough markers, this averages out.
>>These stray random
>>mutations are inherited, and if you have several of them
>>to work with you can build a phylogeny from them and trace lines
>>of descent back to where these random mutations occured
>>if you have enough data to work with.
>
> anybody can do anything with any information. What needs to be
> validated is the premises brought to the data.
What premises exactly are you doubting here? Be specific.
>>>Because of the random nature of mutations
>>>we must use statistics and probability to estimate the Time to the
>>>Most Recent Common Ancestor (TMRCA). The actual calculations of TMRCA
>>>are mathematically complex and depend on knowing the rate of mutation
>>>and the true number of mutations. At this time there is not enough
>>>data to accurately determine either of these factors so certain
>>>assumptions have to be made. The discussion of these assumptions and
>>>the actual calculations are beyond the scope of this webpage."
>>>
>>
>>I'll not comment on TMRCA calculations, they are irrelevant
>>to this discussion.
>
> in what way? This link was given supposedly to support the concept
> that nested hierarchies and lineages can be traced via mutations. The
> link does no such thing. The premise that time to the most recent
> common ancestor can be calculated through mutations does nothing to
> demonstrate a nested hierarchy, as far as I can see. Indeed, it
> un-nests one brother from the other.
No, you fail to understand the nature of nesting. Remember the ape data?
There were a few mutations each that matched each species up with each
other species. That's homoplasy. But the big majority of mutations
matched up the African apes. Any one site could be wrong. But collect
together enough sites and random errors balance out, leaving one clear
signal.
(By the way, I'm afraid that calculation of elapsed time has been
confounded in recent discussions with calculation of branching pattern.
Keep in mind that they are different, and that we are interested in
branching pattern specifically.)
>>>After reviewing your blairgenealogy link, I've come to the conclusion
>>>that it is a lot of pseudo-scientific evo-speak directed at an effort
>>>to validate the evolutionary concept of common descent. It is riddled
>>>with false and faulty premises.
>>
>>I see nothing there about common descent, evolution, or
>>phylogeny. All I see is a few basic biology concepts.
>
> "Time to the most recent common ancestor" surely speaks of common
> descent and evolution over thousands of years, according to the
> article.
Don't confuse time with branching pattern.
>>Point out a faulty premise that you refer too.
>
> the faulty premise is that number of changes in the Y-chromosome must
> mean distance or closeness to a common ancestor. On what basis?
We've covered that. On that basis that mutations happen, and that in the
aggregate their numbers are predictable. This is just like radioactive
decay. You have no idea how long it will take for any one atom to decay,
but you can calculate the half-life of Pu-239 to great precision.
>>I suspect
>>crucial points are missing in your paraphrasing of the article's
>>focus.
>>
>>
>>>To summarize: this is a lot of impressive-looking calculations, based
>>>on false premises, thus making the calculations worthless. Frankly,
>>>it is nonsense and a waste of time.
>>>
>>
>>Point out a calculation based on a false premise. Here's the
>>link again for convenience.
>>
>>http://blairgenealogy.com/dna/dna101.html
>
> The premise is that matched and mismatched markers are indicative of
> closeness or distance from the most recent common ancestor. It is
> assumed, without support, that the number of markers say something
> about the distance from the LCA. On what basis?
Because that's how random mutations work.
Ah, this is different. This calculation is in fact assuming that
mutations in these particular markers are rare enough that we can ignore
them, and that resemblances among relatives only decay because
recombination dilutes them. The calculations here rely on having a
particular distribution of allele frequencies in a panmictic population,
I do believe.
None of this has anything to do with the way we determine relationships
between species, which relies on fixed differences, not polymorphisms.
>>>They need to justify their premises. They have not done so.
>>>
>>
>>So state, for the record, the premise to which you are
>>referring. You use the word "premise" haphazardly on
>>different points, and in this case failed to point out
>>what it is you are referring to.
>
> I think that the faulty premise, in this instance, is that number of
> markers must say something about distance from the last common
> ancestor. And this premise is held so dearly that even when the
> results are off the wall, with one brother being made to be closer to
> the common ancestor than the other, no red flags are raised.
Again, it's a statistical calculation. One marker does not determine
relationships. That's why they use 25 markers, and why there's such a
wide distribution of possible ages. Your inability to distinguish the
behavior of single objects from the behavior of aggregates of many
objects has caused you problems before. Please try hard to understand this.
>>>>When things are copied and errors occur, the replicated copies
>>>>inherit those errors. You find a unique fingerprint in the
>>>>errors when all the descendants are examined.
>>>
>>>similarity in errors do not necessarily mean relationship or common
>>>descent. The same kinds of errors can occur simply because the
>>>template is conducive to the same types of errors occurring.
>>>
>>
>>A few paragraphs earlier your criticism of phylogeny was the
>>randomness of mutations. Now you are claiming they occur
>>according to template?
>
> no, I am saying that the same templates can respond to the environment
> in the same way. I am not saying that there are different templates
> with mutations occurring in the same way to the different templates.
What is a template, in this case? I'm asking about its biological
reality. I see no sign that there are such things as templates in DNA.
>>Biases large enough to produce the phylogenies seen would
>>be easy to spot, why isn't anyone seeing them?
>
> who says no one is seeing them?
Who is seeing them? You certainly aren't.
>>>A Corvette can break down because after, say, 50,000 miles, it needs
>>>its timing belts changed. A Honda can also break down because after
>>>50,000 miles, it needs its timing belts changed. Same problem,
>>>different cars. That doesn't mean that the cars are related. They
>>>just both have similarly designed engines that react to external
>>>stimuli in the same way.
>>>
>>
>>Not relevant unless cars inherit errors.
>
> okay, use computer programs then. Computer programs can inherit and
> pass down viruses. Inheritance is not a sufficient reason to invoke
> the faulty premises.
Huh?
Because that's not the premise and never has been. Nested hierarchy.
>>>>Harshman identified which species
>>>>the nucleotides I posted belonged to *without* using any
>>>>detailed knowledge of the species themselves, and I concealed
>>>>information about which was which.
>>>
>>>again, I am not interested in if John can identify which species the
>>>sequences came from. He needs to justify his premise that similarity
>>>must means relationship and common descent. If there are exceptions
>>>to the similarity standard (and there are many), then his premise is
>>>fatally flawed.
>>>
>>
>>Its not just similarity. I could have posted nucleotides
>>for only Pan and Pongo, similar species, he wouldn't
>>have been able to tell which was which without some detailed
>>knowledge of the nucleotides.
>
> you are still on the identification path. I am still on the
> defense-of-premise path.
Can't defend a premise that isn't a premise.
>>>>In part two of the excercise John
>>>>didn't even have the nucleotides, I just created a tree using the
>>>>nucleotides using the same tool that is being used at
>>>>
>>>>http://www.roperld.com/ycomparison.htm#37Markers
>>>>
>>>>That was also my first use of the tool, I'm a layperson
>>>>like you and not a scientist like John or Steven J. So
>>>>how were we able to pull this off?
>>>
>>>by inputting the info into a program that has the database of these
>>>species, there is no reason why the program should not spit back out
>>>the correct I.D.s But that was not my question.
>>>
>>
>>No database was involved.
>
> really? I've never heard of a program without a database.
I have no idea what you think a database is. But many programs don't
have them. At any rate, you were talking specifically about a database
of species. There is no such database involved. The only program I used
was a phylogenetic analysis program. What it does it take the data it
was given and make a tree out of them according to an algorithm. It has
no idea what the data are, and compares them to nothing except each other.
>>>>We certainly can't do
>>>>this with computer languages or sweaters without corroborating
>>>>amongst ourselves.
>>>
>>>corroboration had to occur for the program to be set up to recognize
>>>the sequences. Those sequences weren't plugged into an empty program
>>>and the identifications were made. There had to be a database
>>>(corroborated by those who have studied the sequences) from which to
>>>pull the matches.
>>>
>>
>>No database, no corroboration, no wizard behind a curtain.
>>John could have done the same thing with pen and paper, its
>>tedious, the software is a labor saver.
>
> and doing it by pen and paper, what would have been his database to
> work from, if not the already identified DNA sequences of the various
> apes and human?
No database at all. Just the sequences themselves, which were not
identified. I constructed a tree using parsimony, which minimizes the
number of mutations required to explain the data. For any sufficiently
consistent set of sequences, there is only one tree on which the number
of required mutations is at a minimum. Then I took that tree and
compared it (still with species unknown) to what I know to be the
correct tree of primates, identifying species in matching positions. And
I could do this because, like I have said many times, analysis of any
sequences will give you the same tree. That's because all the sequences
evolved on the same tree.
>>I could have
>>interchanged some of the ACTG symbols while retaining the
>>patterns of similarites and disimilarities and he still
>>could have done it.
>
> done what? Identified which was which? Nice. But that was not what
> I asked for. I asked for him to defend his premise that similarities
> and dissimilarities invariably must mean relationship or common
> descent.
Not the premise. Nested hierarchy. And what that little demonstration
showed was that nested hierarchy in primates is not arbitrary, as you
had claimed. It's a characteristic of the data themselves, and is
unavoidable. The demonstration showed that when I find that hierarchy
over and over again, I'm not matching anything to my personal
preconceptions of what I ought to find, as you had claimed, because I
can find the same tree even if I have no idea what species is which.
B Richardson
On Sun, 14 Aug 2005 03:57:30 EDT, B Richardson wrote:
>snip>
>
>zoe wrote:
>
>>>Also, the following comment taken from your link is reminiscent of
>>>what I read in Nature back in 2002. See sublink from the above link:
>>>
>>>http://blairgenealogy.com/dna/dna101.html
>>>
>>>"Mutations occur at random. This means IT IS POSSIBLE FOR TWO DISTANT
>>>COUSINS TO MATCH EXACTLY ON ALL MARKERS WHILE TWO BROTHERS MIGHT NOT
>>>MATCH EXACTLY. (Caps mine.)
>>
>>And the brother that has picked up another marker not shared
>>by the other brother and distant cousin now can have a line
>>of descent traceable to uniquely him.
>
>this, to me, is nonsense.
Why? The brother with the marker that doesn't match with his
other brother or distant cousin will pass it on to his
descendants. His descendants can then be distinguished
from the those of his brother and also his distant cousin
by examining this marker. This is pretty basic stuff.
>Just because one brother shows up with some
>extra mutations does not mean that he alone is of a lineage further
>removed or closer than that of his other brother.
Of course not. I really don't see how you can manage to
get that out of what I wrote.
> Son A and Son B
>were both born of the same parents. Regardless of what changes there
>are in the two sons, it does not make one son closer or further away
>from his parents than the other. Many generations down the road,
>offspring descended from Sons A and B will not have some members that
>are closer or further from A and B's parents than their siblings.
>
Irrelevent. Any two given lineages can be approximately equidistant
from an LCA, but that isn't interesting. Their lines of descent
is what we're interested in. You can ascertain that two descendants
of son A are more closely related to each other than either of them
is to descendants of son B by examining the marker.
>
>So on what basis does the genealogist decide that one member is
>further removed than another?
>
Lets use the same example, the two brothers and the distant
cousin. Brother A picks up a marker Z not shared by the
other brother or distant cousin. Generations later, a carrier
of marker Z picks up a marker W, and later in the ZW lineage a
mutation produces marker U. Say a descendant in the lineage
of brother B picks up a marker P, and later in the lineage
a carrier of marker P picks up a marker Q.
If a individual is carrying markers Z and W, he is more closely
related to an individual carrying the Z (but no W) marker than
he is to an individual with the P marker. An individual with
markers P and Q would also be more distantly related to an individual
with markers Z and W than he is to an individual with the P
marker but no Q.
>
>> These stray random
>>mutations are inherited, and if you have several of them
>>to work with you can build a phylogeny from them and trace lines
>>of descent back to where these random mutations occured
>>if you have enough data to work with.
>
>anybody can do anything with any information.
Then show an example where a nested hierarchy is recoverable
from data that did not result from replication with error.
Thats all it would take to give your argument some merit.
With the examples you give like sweaters, fanbelts and programming
languages, you have failed to produce a substansive point.
> What needs to be
>validated is the premises brought to the data.
>
What premises? You rarely state the premises you say
are false, and when you do they are badly mangled and
have little resemblance to the actual claims you are
attempting to dispute. How about the nested hierarchy
exists and is recoverable from genetic data? Do you
dispute that?
>
>snip>
>
>>> Because of the random nature of mutations
>>>we must use statistics and probability to estimate the Time to the
>>>Most Recent Common Ancestor (TMRCA). The actual calculations of TMRCA
>>>are mathematically complex and depend on knowing the rate of mutation
>>>and the true number of mutations. At this time there is not enough
>>>data to accurately determine either of these factors so certain
>>>assumptions have to be made. The discussion of these assumptions and
>>>the actual calculations are beyond the scope of this webpage."
>>>
>>
>>I'll not comment on TMRCA calculations, they are irrelevant
>>to this discussion.
>
>in what way?
In what way would they be? You can reproduce a phylogenetic
tree without doing them.
> This link was given supposedly to support the concept
>that nested hierarchies and lineages can be traced via mutations.
No, I produced a link that had a list of pet geneology
projects to satisfy your request for a references that
human geneologies documented by historical record can
be tracked via phylogenetic analysis. You scoured the
page and fished out a link to another site (the blairgeneology
DNA101 primer), posted that link, and then insinuated that
I claimed every item on the link *you* posted is directly
relevant to producing a basic phylogenetic tree from genetic
data. You then proceeded to dismiss the link *you*
posted as "pseudo-scientific evo-speak" and "a worthless
waste of time". I'm not knocking the link, it looks like
an acceptable primer to me, but I had not seen it until
you posted it.
> The
>link does no such thing. The premise that time to the most recent
>common ancestor can be calculated through mutations does nothing to
>demonstrate a nested hierarchy, as far as I can see.
Thats why I said TMRCA calculations were irrelevent. The premise
that TMRCA demonstrates a nested hierarchy is yours. The
blairgeneology link doesn't claim that it does, I don't
claim that it does. You're arguing with stuff you're making up.
> Indeed, it
>un-nests one brother from the other.
>
That statement isn't wrong, its meaningless. You seem to have
a fixation on a phylogeny with only two branches, and
similarites/dissimilarites of only two species or brothers.
All you can tell with two branches is that the nodes are
equidistant from each other which isn't useful. You need
three or more to be nested.
>
>>>After reviewing your blairgenealogy link, I've come to the conclusion
>>>that it is a lot of pseudo-scientific evo-speak directed at an effort
>>>to validate the evolutionary concept of common descent. It is riddled
>>>with false and faulty premises.
>>>
>>
>>I see nothing there about common descent, evolution, or
>>phylogeny. All I see is a few basic biology concepts.
>
>"Time to the most recent common ancestor" surely speaks of common
>descent and evolution over thousands of years, according to the
>article.
>
Where does the article say that TMRCA "surely speaks of common
descent and evolution over thousands of years"? Not agreeing
or disagreeing, I just don't see it at the page. Is something
mangled in the paraphrasing here?
>>
>>Point out a faulty premise that you refer too.
>
>the faulty premise is that number of changes in the Y-chromosome must
>mean distance or closeness to a common ancestor. On what basis?
>
Lets get back to the brothers A and B. Son of A (lets call him A1) has
acquired marker Z, grandson of A1 acquires marker W, great great
grandson of A1 acquires marker U. Grandson of B acquires marker P,
his grandson acquires marker Q. Both brothers inherit marker K
from their father. Say I have five samples from the descendants
of A and B and they have the markers
KZ
KZU
KZUW
KP
KPQ
One can easily tell that KP and KPQ are more closely to related to each
other than either of the are to anybody carrying the Z marker. I can
also deduce KZUW shares a more recent ancestor with KZU than it does with
KZ, and also shares a more recent ancestor with KZ that he does with
KP or KPQ. Thus the relationship looks like
|-------KZ
|---+
| | |---KZU
| |---+
| |---KZUW
+
| |-------KP
|---+
|-------KPQ
There is more distance between KPQ and KZUW than there is between
KP and KPQ. We have no reason to be concerned with exact distances
for this phylogeny. We're also not concerned to distances to LCA,
but relative distances between nodes. If you can't easily make
multiple inferences about relation from the cladogram at this point
I'm at a loss of how to make it simpler.
>
>snip>
>
>> I suspect
>>crucial points are missing in your paraphrasing of the article's
>>focus.
>>
>>>
>>>To summarize: this is a lot of impressive-looking calculations, based
>>>on false premises, thus making the calculations worthless. Frankly,
>>>it is nonsense and a waste of time.
>>>
>>
>>Point out a calculation based on a false premise. Here's the
>>link again for convenience.
>>
>>http://blairgenealogy.com/dna/dna101.html
>
>The premise is that matched and mismatched markers are indicative of
>closeness or distance from the most recent common ancestor. It is
>assumed, without support, that the number of markers say something
>about the distance from the LCA. On what basis?
>
See the cladogram above. You should be able to make several inferences
about relationship (i.e. some given branch is more closely or more distantly
related to some second branch than it is to a third branch). You should
also be able to note that if you pick only pairs of branches that you
can't tell which is closer to which. If you can't I don't know of
a simpler way to put it. Also, were not concerned with distances to LCA,
were concerned with the relative distances between nodes on a
tree with more than two brances.
I didn't ask for a badly munged cut and paste job, I asked for
the faulty calculations and premises you referred to. If you're
trying to make a point, you forgot to include it. Which calculation
or premise is faulty? And also, why is this table from the link
*you* posted relevant to this discussion about phylogeny?
>
>>>They need to justify their premises. They have not done so.
>>>
>>
>>So state, for the record, the premise to which you are
>>referring. You use the word "premise" haphazardly on
>>different points, and in this case failed to point out
>>what it is you are referring to.
>
>I think that the faulty premise, in this instance, is that number of
>markers must say something about distance from the last common
>ancestor.
Markers are cumulative, more generations = more markers.
Seems to be a reasonable premis to me. Also, we're not
concerned with distances to LCA, were concerned with
the relative distances between nodes where more than
two nodes exist.
> And this premise is held so dearly that even when the
>results are off the wall, with one brother being made to be closer to
>the common ancestor than the other, no red flags are raised.
>
I see nothing on that link you fished out that suggests
one brother is more related to an ancestor that the other
brother, you've aparrantly badly paraphrased it. All I see
is that one brother can acquire a marker that the other
brother and distant cousin doesn't have. These markers
are acquired at random, and can be used to identify lineages.
There is nothing in that little tidbit about the brothers
and distant cousin that supports your argument. Also exact
distances to LCA doesn't concern us, we're interested in
relative distances between nodes on a tree with more than two
branches. Why did you post the blairgeneology link? Nothing
on it supports your arguments.
>
>snip>
>
>>>>When things are copied and errors occur, the replicated copies
>>>>inherit those errors. You find a unique fingerprint in the
>>>>errors when all the descendants are examined.
>>>
>>>similarity in errors do not necessarily mean relationship or common
>>>descent. The same kinds of errors can occur simply because the
>>>template is conducive to the same types of errors occurring.
>>>
>>
>>A few paragraphs earlier your criticism of phylogeny was the
>>randomness of mutations. Now you are claiming they occur
>>according to template?
>
>no, I am saying that the same templates can respond to the environment
>in the same way. I am not saying that there are different templates
>with mutations occurring in the same way to the different templates.
>
Plenty of studies have been done on mutations, produce a reference
that supports your claim. You've also protested loudly in
this very thread that the randomness of mutations disqualifies
any notion of descent producing a phylogeny. Now you are
claiming that the phylogeny, which you dispute exists, is because
identical templates (whatever that means) have identical responses
to environmental stimuli. The two notions are diametrically opposed.
You also produced an additional problem for yourself now, in
addition to the mutations occuring precisely to a "template"
and environmental stimuli, they must also fixate in a precise
manner across entire clades. Can you produce any relevant
studies that support this notion with data produced by
observation or experiment?
>
>>Biases large enough to produce the phylogenies seen would
>>be easy to spot, why isn't anyone seeing them?
>
>who says no one is seeing them?
>
I am. Biases in mutations *and* fixation an a scale required to
produce the phylogenies seen just isn't there. You can always
flood me with references that show I'm wrong.
>
>>>A Corvette can break down because after, say, 50,000 miles, it needs
>>>its timing belts changed. A Honda can also break down because after
>>>50,000 miles, it needs its timing belts changed. Same problem,
>>>different cars. That doesn't mean that the cars are related. They
>>>just both have similarly designed engines that react to external
>>>stimuli in the same way.
>>>
>>
>>Not relevant unless cars inherit errors.
>
>okay, use computer programs then. Computer programs can inherit and
>pass down viruses.
Which typically replicate perfectly. If those viruses acquire
errors at random and pass them on to replicated copies, you
can reproduce the evolutionary history of a computer virus
with phylogenetic analysis.
> Inheritance is not a sufficient reason to invoke
>the faulty premises.
>
If you intended to criticize phylogenetic analysis with
your comment about inheritance, you omitted some verbage.
What faulty premises?
He has demonstrated that the nested hierarchy is recoverable
from randomly chosen genes. At the moment descent is the only
working hypothesis that survives consistancy checks that has been
able to explain it.
>
>>>>Harshman identified which species
>>>>the nucleotides I posted belonged to *without* using any
>>>>detailed knowledge of the species themselves, and I concealed
>>>>information about which was which.
>>>
>>>again, I am not interested in if John can identify which species the
>>>sequences came from. He needs to justify his premise that similarity
>>>must means relationship and common descent. If there are exceptions
>>>to the similarity standard (and there are many), then his premise is
>>>fatally flawed.
>>>
>>
>>Its not just similarity. I could have posted nucleotides
>>for only Pan and Pongo, similar species, he wouldn't
>>have been able to tell which was which without some detailed
>>knowledge of the nucleotides.
>
>you are still on the identification path. I am still on the
>defense-of-premise path.
>
Your path is getting a bit twisted. You claimed the randomness
of mutations prevented phylogenetic analysis from being meaningful.
Then you insinuated that mutations occur very precisely according
to some template. The statements are diametrically opposed and
neither is true. You also posted a link, attributed it to me
and then proceeded to garble notions on the page and claim
it supports you criticisms of phylogeny.
How did John identify the species if it was a means other than
the telltale signal left by descent? What premise are you referring
to?
>
>>>>In part two of the excercise John
>>>>didn't even have the nucleotides, I just created a tree using the
>>>>nucleotides using the same tool that is being used at
>>>>
>>>>http://www.roperld.com/ycomparison.htm#37Markers
>>>>
>>>>That was also my first use of the tool, I'm a layperson
>>>>like you and not a scientist like John or Steven J. So
>>>>how were we able to pull this off?
>>>
>>>by inputting the info into a program that has the database of these
>>>species, there is no reason why the program should not spit back out
>>>the correct I.D.s But that was not my question.
>>>
>>
>>No database was involved.
>
>really? I've never heard of a program without a database.
>
Really.
>
>>>> We certainly can't do
>>>>this with computer languages or sweaters without corroborating
>>>>amongst ourselves.
>>>
>>>corroboration had to occur for the program to be set up to recognize
>>>the sequences. Those sequences weren't plugged into an empty program
>>>and the identifications were made. There had to be a database
>>>(corroborated by those who have studied the sequences) from which to
>>>pull the matches.
>>>
>>
>>No database, no corroboration, no wizard behind a curtain.
>>John could have done the same thing with pen and paper, its
>>tedious, the software is a labor saver.
>
>and doing it by pen and paper, what would have been his database to
>work from, if not the already identified DNA sequences of the various
>apes and human?
>
No database. The identities of the sequences were concealed.
>
>>I could have
>>interchanged some of the ACTG symbols while retaining the
>>patterns of similarites and disimilarities and he still
>>could have done it.
>
>done what? Identified which was which? Nice. But that was not what
>I asked for. I asked for him to defend his premise that similarities
>and dissimilarities invariably must mean relationship or common
>descent.
>
That wasn't his premise. He claimed that the same tree could
be produced for any gene and asked why that was the case. The
phrase "similarities and dissimilarites invariably must mean
relationship" came from you and you alone, but you attributed
it to Harshman.
>
>snip>
>
>
>