questions for Seanpit about amino acids
geo...@hotmail.com
is that, the larger they get, the fewer viable sequences there are of
that size to mutate to.
I don't believe that size is the problem here, so I'd like to ask you
a few questions about how these systems work.
1) If I have a 300aa system, and that system is duplicated, is the
result:
a) a 600aa system?
b) just 'two 300aa systems next to each other'?
c) something else?
If (a), then doesn't this prove that the size of a system is
irrelevent to the ease of obtaining it?
If (b), then I have further questions.
2) If (b) was true, then this is just a couple of 300aa systems. Call
them A and B. You claim that both of them have a larger number of
viable systems they could mutate to, because they're smaller.
But now, suppose that a mutation in A makes it reliant on B. This
could easily happen because B is providing the same functions as A,
which allows A to give up some function and mutate it to something
else.
Is the system now:
a) a 600aa system?
b) still just two 300aa systems?
c) something else?
If (a), then again, isn't it quite trivial to get these high aa
systems?
If (b), then doesn't that mean that all high aa systems can be
regarded as several low aa subsystems?
3) If (b) was true, then in theory, a 1000aa system can be a sum of
many subsystems, and those subsystems may be considered low aa
systems. In this case, doesn't this mean that a 1000aa system can
easily find viable mutation possibilities, simply by mutations in its
subsystems (which have many possibilities available)?
Venus
Seanpit
> As I understand it, your whole problem with these amino acid systems
> is that, the larger they get, the fewer viable sequences there are of
> that size to mutate to.
Size is only half of the problem. The other half is sequence
specificity. Just because a system has a large number of residues
doesn't mean that there is a significant degree of specificity for the
arrangement of the residues relative to each other. A large system
with low specificity can be on a much lower level of complexity than a
much smaller system with a higher degree of specificity.
> I don't believe that size is the problem here, so I'd like to ask you
> a few questions about how these systems work.
>
> 1) If I have a 300aa system, and that system is duplicated, is the
> result:
>
> a) a 600aa system?
Not necessarily. It is a 600aa sequence, but this sequence isn't
necessarily going to have a beneficial system of function attached to
it.
> b) just 'two 300aa systems next to each other'?
That can happen as well. Simple duplication doesn't make anything
new. It just makes more of the same thing. It is quantitative, not
qualitative, mutation.
> c) something else?
>
> If (a), then doesn't this prove that the size of a system is
> irrelevent to the ease of obtaining it?
Simply producing a larger sequence with a multicharacter mutation
isn't enough to find a novel type of beneficial function that requires
at least that many fairly specified amino acid residues.
For example, say that there is a specific 10-letter sequence that, if
found, would win you a million dollars. You know what the first 5
letters are. What are the odds that simply doubling your first five
letters, to make a 10-letter sequence, is going to end up being the
winning 10-letter sequence?
See the point of the problem here?
> If (b), then I have further questions.
>
> 2) If (b) was true, then this is just a couple of 300aa systems. Call
> them A and B. You claim that both of them have a larger number of
> viable systems they could mutate to, because they're smaller.
That's right. The odds of finding a novel beneficial 300aa target are
exponentially greater than the odds of finding a novel 1000aa target
because the ratio of targets vs. non-targets is exponentially greater
at the 300aa level vs. the 1000aa level.
> But now, suppose that a mutation in A makes it reliant on B. This
> could easily happen because B is providing the same functions as A,
> which allows A to give up some function and mutate it to something
> else.
>
> Is the system now:
>
> a) a 600aa system?
Nope. It is still just a 300aa system that only became beneficial
because of a certain type of environment - an environment that
includes everything that already exists in a given genome.
> b) still just two 300aa systems?
Right . . .
> c) something else?
>
> If (a), then again, isn't it quite trivial to get these high aa
> systems?
>
> If (b), then doesn't that mean that all high aa systems can be
> regarded as several low aa subsystems?
No, because there are systems, like the flagellar system for example,
that require many thousands of fairly specified residues to be working
together at the same time in a specific orientation with each other
for the overall system to work. This is not the case with your two
separately acting 300aa systems. Because each residue in your two
systems does not have to be specifically arranged with all the other
599 residues, this system is not very specified. It is therefore not
any more functionally complex than the most complex intact or
specified portion of the system - in this case 300 fsaars. This is
why equally large cascading systems made up of, say, 5 different
proteins, are not as functionally complex as a 5-protein system of
equivalent numbers of residues where all the individual protein parts
must be specifically arranged with each other in 3D space (and
therefore all of the residues as well).
> 3) If (b) was true, then in theory, a 1000aa system can be a sum of
> many subsystems, and those subsystems may be considered low aa
> systems. In this case, doesn't this mean that a 1000aa system can
> easily find viable mutation possibilities, simply by mutations in its
> subsystems (which have many possibilities available)?
You'd be correct if you were talking about a cascading system of
function where each part was not required to be specifically arranged
in 3D space with all the other parts at the same time.
> Venus
Sean Pitman
www.DetectingDesign.com
hersheyh
wrote:[snip]
>
> That's right. The odds of finding a novel beneficial 300aa target are
> exponentially greater than the odds of finding a novel 1000aa target
> because the ratio of targets vs. non-targets is exponentially greater
> at the 300aa level vs. the 1000aa level.
You say "exponentially greater". How much greater is that? Let's use
333aa and 1000aa systems. The 1000aa system is linearly 3 times
larger than the 333aa system. How many times larger is the
"exponential" difficulty of finding a beneficial target in the 1000aa
system than in the 333aa system that is 1/3 the size? Nine? Twenty-
seven? Tell me what *you* mean by "exponentially greater"?
>
[snip]
geo...@hotmail.com
wrote:
> On 28 Nov, 10:24, geop...@hotmail.com wrote:
>
> > As I understand it, your whole problem with these amino acid systems
> > is that, the larger they get, the fewer viable sequences there are of
> > that size to mutate to.
>
> Size is only half of the problem. The other half is sequence
> specificity. Just because a system has a large number of residues
> doesn't mean that there is a significant degree of specificity for the
> arrangement of the residues relative to each other. A large system
> with low specificity can be on a much lower level of complexity than a
> much smaller system with a higher degree of specificity.
>
> > I don't believe that size is the problem here, so I'd like to ask you
> > a few questions about how these systems work.
>
> > 1) If I have a 300aa system, and that system is duplicated, is the
> > result:
>
> > a) a 600aa system?
>
> Not necessarily. It is a 600aa sequence, but this sequence isn't
> necessarily going to have a beneficial system of function attached to
> it.
I should add here that I'm basically equating 'gene sequences' to
'amino acid residues' (amino acid chains formed by concatenation of
the amino acids output by translated DNA), but after a little research
I see what you mean, and that the two don't quite mean the same
My idea is that a sequence of DNA can be duplicated, which causes a
structure to duplicate also, whether it's a whole protein or a piece
of one. I believe what you're suggesting is that a duplication inside
a protein would change its shape to something weird and make it
unfunctional?
If that's the case then I'm at the limit of my knowledge here, so I'll
have to accept you may be correct. However, I've found that stuff is
rarely black and white. It's a little like the whole evolution debate
in microcosm, except instead of 'what use is half an eye?' it's now
'what use is half a protein'? Despite what Behe claims, I don't
believe stuff is much more 'irreducible' at the molecular level.
>
> > b) just 'two 300aa systems next to each other'?
>
> That can happen as well. Simple duplication doesn't make anything
> new. It just makes more of the same thing. It is quantitative, not
> qualitative, mutation.
>
> > c) something else?
>
> > If (a), then doesn't this prove that the size of a system is
> > irrelevent to the ease of obtaining it?
>
> Simply producing a larger sequence with a multicharacter mutation
> isn't enough to find a novel type of beneficial function that requires
> at least that many fairly specified amino acid residues.
>
> For example, say that there is a specific 10-letter sequence that, if
> found, would win you a million dollars. You know what the first 5
> letters are. What are the odds that simply doubling your first five
> letters, to make a 10-letter sequence, is going to end up being the
> winning 10-letter sequence?
>
> See the point of the problem here?
>
I can see yours, but I'm not sure I've made mine clear. It's not a
question of probability if there's a multitude of goals.
> > If (b), then I have further questions.
>
> > 2) If (b) was true, then this is just a couple of 300aa systems. Call
> > them A and B. You claim that both of them have a larger number of
> > viable systems they could mutate to, because they're smaller.
>
> That's right. The odds of finding a novel beneficial 300aa target are
> exponentially greater than the odds of finding a novel 1000aa target
> because the ratio of targets vs. non-targets is exponentially greater
> at the 300aa level vs. the 1000aa level.
>
> > But now, suppose that a mutation in A makes it reliant on B. This
> > could easily happen because B is providing the same functions as A,
> > which allows A to give up some function and mutate it to something
> > else.
>
> > Is the system now:
>
> > a) a 600aa system?
>
> Nope. It is still just a 300aa system that only became beneficial
> because of a certain type of environment - an environment that
> includes everything that already exists in a given genome.
I don't get your meaning here.
Well, I believe that most arrangements are more like this and not
quite as specific as you believe, seeing as the argument from
specificity often fails when applied to other stuff when it fails to
consider every option. However, I'd have to ask a molecular biologist
about that.
Thanks for answering the questions.
>
> > Venus
>
> Sean Pitmanwww.DetectingDesign.com
heekster
<seanpi...@naturalselection.0catch.com> wrote:
<snippage>
>That's right. The odds of finding a novel beneficial 300aa target are
>exponentially greater than the odds of finding a novel 1000aa target
"Exponentially greater", as used above, is a mathematical imbecility,
and it has no meaning, without additional clarification. The
statement is an absurdity, because the probablity, "the odds", range
between 0 and unity. The statement is also, just an assertion. No
proof has been offered to support the premise.
>because the ratio of targets vs. non-targets is exponentially greater
>at the 300aa level vs. the 1000aa level.
>
"Exponentially greater", as used above, is a mathematical imbecility,
and it has no meaning, without additional clarification. Again, there
has been no attempt to substantiate and prove the assertion.
An exponential function has the form y = a to the x power, where a,
the base, is a positive number typically greater than 1. Exponential
functions are continuous and defined for all values of x.
Exponential functions possess the property of exponential growth.
We say that a quantity grows "exponentially" when it grows at a rate
that is proportional to its size.
The statement quoted above, does not make sense, wrt exponentials.
Seanpit
Not necessarily. It just is unlikely to hit upon a new type of
function, a function that was not already in the genome pool to begin
with, that requires at least 600aa at minimum to work. And, this
likelihood only gets exponentially more and more unlikely as you
consider higher and higher level functional systems.
It is kinda like knowing the first 10 numbers in a 20 number lottery
and expecting to get the next 10 numbers "right" simply by duplicating
the first 10. Possible? Yes. Likely? No.
> If that's the case then I'm at the limit of my knowledge here, so I'll
> have to accept you may be correct. However, I've found that stuff is
> rarely black and white. It's a little like the whole evolution debate
> in microcosm, except instead of 'what use is half an eye?' it's now
> 'what use is half a protein'? Despite what Behe claims, I don't
> believe stuff is much more 'irreducible' at the molecular level.
Half a protein may be very useful. The point here is that most
potential protein-sequences and collections of sequences are not or
would not be useful to any beneficial degree from the perspective of
any particular life form. And, this ratio only gets exponentially
worse and worse at higher and higher levels of functional complexity.
> > > b) just 'two 300aa systems next to each other'?
>
> > That can happen as well. Simple duplication doesn't make anything
> > new. It just makes more of the same thing. It is quantitative, not
> > qualitative, mutation.
>
> > > c) something else?
>
> > > If (a), then doesn't this prove that the size of a system is
> > > irrelevent to the ease of obtaining it?
>
> > Simply producing a larger sequence with a multicharacter mutation
> > isn't enough to find a novel type of beneficial function that requires
> > at least that many fairly specified amino acid residues.
>
> > For example, say that there is a specific 10-letter sequence that, if
> > found, would win you a million dollars. You know what the first 5
> > letters are. What are the odds that simply doubling your first five
> > letters, to make a 10-letter sequence, is going to end up being the
> > winning 10-letter sequence?
>
> > See the point of the problem here?
>
> I can see yours, but I'm not sure I've made mine clear. It's not a
> question of probability if there's a multitude of goals.
Yes, it is. There are a great many potential targets or "winning
numbers" within the lottery of sequence space at each level of
functional complexity - trillions upon trillions of them even for 100
fsaar systems. The problem, of course, is that there are a great many
more non-beneficial sequences. The odds of ending up upon any one of
them involved probability analyzes.
> > > If (b), then I have further questions.
>
> > > 2) If (b) was true, then this is just a couple of 300aa systems. Call
> > > them A and B. You claim that both of them have a larger number of
> > > viable systems they could mutate to, because they're smaller.
>
> > That's right. The odds of finding a novel beneficial 300aa target are
> > exponentially greater than the odds of finding a novel 1000aa target
> > because the ratio of targets vs. non-targets is exponentially greater
> > at the 300aa level vs. the 1000aa level.
>
> > > But now, suppose that a mutation in A makes it reliant on B. This
> > > could easily happen because B is providing the same functions as A,
> > > which allows A to give up some function and mutate it to something
> > > else.
>
> > > Is the system now:
>
> > > a) a 600aa system?
>
> > Nope. It is still just a 300aa system that only became beneficial
> > because of a certain type of environment - an environment that
> > includes everything that already exists in a given genome.
>
> I don't get your meaning here.
Two 300aa systems that work together to produce a certain product or
function, but that are not required to be specifically oriented with
each other in 3D space, are like cascading systems. The level of
functional complexity for such systems is not significantly greater
than the complexity level of the single specified part of the system -
i.e., 300aa in this case.
Cascading systems are like this. However, many systems are not.
Again, consider the bacterial rotary flagellar motility system. All
of the protein parts of this system are indeed required to be
specifically arranged relative to all of the other parts in the system
at the same time in 3D space. Such a system is far far more
functionally complex that a system of the same number of residues that
does not require all of its protein parts to be specifically arranged
relative to each other - as in a cascading enzymatic system. Such
cascading systems are no more complex than the most complex single
specified part of the system.
> Thanks for answering the questions.
You're welcome . . .
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Mon, 1 Dec 2008 15:21:46 -0800 (PST), Seanpit
>
http://www.detectingdesign.com/flagellum.html#Calculation
Sean Pitman
www.DetectingDesign.com
'Rev Dr' Lenny Flank
Hey Sean, if the gap between jaguars and cheetahs isn't too large to
be crossed in sequence space, then why is the much smaller gap between
humans and chimps too large top be crossed in sequence space?
If sequence spaces cannot be crossed from one point to another, then
how does ANY new species form? Why is the crossing of sequence space
from point "ape" to point "human" any less likely than the often-much-
larger gap from ANY species A to ANY species B?
Other than your religious opinion that humans simply are too divinely
"special" to have evolved?
================================================
Lenny Flank
"There are no loose threads in the web of life"
Editor, Red and Black Publishers
http://www.RedandBlackPublishers.com
'Rev Dr' Lenny Flank
> Not necessarily. It just is unlikely to hit upon a new type of
> function, a function that was not already in the genome pool to begin
> with, that requires at least 600aa at minimum to work. And, this
> likelihood only gets exponentially more and more unlikely as you
> consider higher and higher level functional systems.
Then how does ANY species evolve, Sean?
Don't they ALL cross sequence space from one point to another? And
aren't most of the speices that creationists acept have "micro-
evolved" (like, say, jaguars and cheetahs) FURTHER APART in "sequence
space" than humans and chimps are?
So why is the gap between jaguars and cheetahs in "sequence space"
easily crossed, but the MUCH SMALLER gap in "sequence space" from
chimp to human is impossible to cross?
Besides, I mean, your religious opinion that humans simply cannot have
Seanpit
There is a linear increase in the likely gap distance between anything
in a particular genome and the likely distance to the closest
potentially beneficial sequence (i.e., target) at a particular degree
of minimum specificity with increasing sequence size requirements.
Each linear increase in the gap distance translates into an
exponential increase in the number of random mutations needed to cross
the gap by 20 fold. So, if the gap distance increased from 1 to 50 as
the threshold increased from 333 fsaar to 1000, the number of
mutations needed to cross the gap would increase by 20^N - - or 20^50
in this case.
For further detail see:
'Rev Dr' Lenny Flank
>
> Yes, it is. There are a great many potential targets or "winning
> numbers" within the lottery of sequence space at each level of
> functional complexity - trillions upon trillions of them even for 100
> fsaar systems. The problem, of course, is that there are a great many
> more non-beneficial sequences. The odds of ending up upon any one of
> them involved probability analyzes.
That's nice.
Why,. again, is the "probability" of a jaguar evolving from another
cat (a cheetah, say) greater than the "probability" of a human
evolving from a (much mnore closely genetically-related) chimp?
Show me your math, Sean.
'Rev Dr' Lenny Flank
> http://www.detectingdesign.com/flagellum.html#Calculation
>
Given your math and assumptions, Sean, it would seem to be impossible,
in your view, for ANY species to have evolved from ANY other species.
Is that your view?
If so, why does every other creationist (excpet Ray) think that view
is silly?
If not, then what makes the evolution through "sequence space" of a
human from a chimp any less likely than any OTHER species evolving
from a more-genetically-distant ancestor? Why is it more likely for
other species to cross larger genetic gaps than it is for humans and
chimps to cross their much-smaller gap?
Other than your religious opinion that humans are too godly to have
evolved?
Seanpit
> (snip lots of arm-waving)
>
> Hey Sean, if the gap between jaguars and cheetahs isn't too large to
> be crossed in sequence space, then why is the much smaller gap between
> humans and chimps too large top be crossed in sequence space?
As I've pointed out to you before, you have no basis to argue that the
gap between jaguars and cheetahs is larger than between humans and
apes. Jaguars and cheetahs are clearly part of the same genetic pool
of options - nothing but Mendelian variations on the same theme. In
short, they can breed and produce viable and fertile offspring.
Humans and apes cannot produce viable much less fertile offspring -
indicating significant functional gene pool differences.
As noted before for you, these differences are likely the result of
functional non-coding sequences within the genomes that is often quite
different and unique between humans and apes. It seems that
functional complexity at such very high levels is based more on non-
coding DNA than coding DNA - much much more. Genomic sizes of various
creatures reflect this hypothesis with many simpler forms having
similar numbers of genes, but far less non-coding DNA (formerly known
as 'junk-DNA'). Emergent functional "complexity" therefore seems to be
much more closely related to the amount of non-coding DNA vs. coding
DNA.
Beyond this, however, not enough information is known as to the actual
functional genetic differences between humans and apes.
> If sequence spaces cannot be crossed from one point to another, then
> how does ANY new species form? Why is the crossing of sequence space
> from point "ape" to point "human" any less likely than the often-much-
> larger gap from ANY species A to ANY species B?
You need to deal with specific functional systems for which there is
enough known information to answer such questions. Knowledge of the
functional aspects of the human and/or ape genomes is not sufficient
yet.
> Other than your religious opinion that humans simply are too divinely
> "special" to have evolved?
Not at all. Based on what is currently known, a common evolutionary
ancestor of humans and apes cannot be adequately excluded on a genetic
basis.
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
> Editor, Red and Black Publishershttp://www.RedandBlackPublishers.com
Sean Pitman
www.DetectingDesign.com
Seanpit
Why do you keep re-posting the same stuff over and over again in the
very same thread before I even have a chance to respond? Come on
now . . .
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Dec 1, 10:55 pm, Seanpit <sean...@gmail.com> wrote:
>
>
>
> > Yes, it is. There are a great many potential targets or "winning
> > numbers" within the lottery of sequence space at each level of
> > functional complexity - trillions upon trillions of them even for 100
> > fsaar systems. The problem, of course, is that there are a great many
> > more non-beneficial sequences. The odds of ending up upon any one of
> > them involved probability analyzes.
>
> That's nice.
>
> Why,. again, is the "probability" of a jaguar evolving from another
> cat (a cheetah, say) greater than the "probability" of a human
> evolving from a (much mnore closely genetically-related) chimp?
Mendelian variation isn't the evolution of anything new, functionally
new, within the genome of a qualitative nature. Big cat variations
are not based on anything other than Mendelian variation - not real
evolution of novel genetic functional features within the genome.
This could also be true of humans and apes, but is less likely due to
the fact that humans and apes cannot produce viable much less fertile
hybrid offspring. There are also likely functional brain differences
as well, down to the cellular level, which are likely based on
significant differences in functional non-coding DNA sequences.
> Show me your math, Sean.
>
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
'Rev Dr' Lenny Flank
> On 1 Dec, 20:04, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
> > (snip lots of arm-waving)
>
> > Hey Sean, if the gap between jaguars and cheetahs isn't too large to
> > be crossed in sequence space, then why is the much smaller gap between
> > humans and chimps too large top be crossed in sequence space?
>
> As I've pointed out to you before, you have no basis to argue that the
> gap between jaguars and cheetahs is larger than between humans and
> apes.
Um, humans and chimps are 98.5% identical in their DNA.
That is closer than most of the other species which creationists
assume "microevolved".
So YOU tell ME how YOU measure the genetic gap, then, and by what
measure "humans" and "chimps" are FURTHER APART than most other
speices . . . . . . .?
Other than your religious opinion that humans are special and MUST be
"different" from all other species . . . .
Jaguars and cheetahs are clearly part of the same genetic pool
> of options - nothing but Mendelian variations on the same theme.
And since humans and chimps are 98.5% identical in their DNA ---
closer together than horses and donkeys, or jaguars and cheetahs, they
too are clearly part of the same genetic pool of options -- nothing
but Mendelian variations on the same theme.
In
> short, they can breed and produce viable and fertile offspring.
> Humans and apes cannot produce viable much less fertile offspring -
> indicating significant functional gene pool differences.
So what. Domestic wheat and wild emmer grass can't interbreed and
produce fertile offspring, yet we know for a historical fact that
domestic wheat is descended from wild emmer grass. The grey tree frog
Hyla chrysoscelis is so identical to the grey tree frog Hyla
versicolor that they can't be identified in the field, yet they too
are utterly incapable of producing fertile offspring.
So why is it possible for emmer and wheat, or for H chrysoscelis and H
versicolor, to cross those "signfiicant functional gene pool
differences", but not for humans and chimps to do the same? Why is
it, in your view, that emmer grass can cross the "sequence space" to a
different species that can't interbreed with it, but chimps could not
cross the (much closer) "sequence space" to humans?
Other than your religious assumption that humans are divine and cannot
have evolved.
>
> As noted before for you, these differences are likely the result of
> functional non-coding sequences within the genomes that is often quite
> different and unique between humans and apes. It seems that
> functional complexity at such very high levels is based more on non-
> coding DNA than coding DNA - much much more. Genomic sizes of various
> creatures reflect this hypothesis with many simpler forms having
> similar numbers of genes, but far less non-coding DNA (formerly known
> as 'junk-DNA'). Emergent functional "complexity" therefore seems to be
> much more closely related to the amount of non-coding DNA vs. coding
> DNA.
That's nice.
How is that different in any other species?
Why is nit that OTHER specvies can cross "sequence space" to new
species, but only HUMANS can't have crossed the (much smaller)
"sequence space" betwen them and apes?
Other than your religious opinion that humans simply can not have
evolved from anything, period?
>
> Beyond this, however, not enough information is known as to the actual
> functional genetic differences between humans and apes.
Then, uh, how the hell can you calculate its probability in sequence
space?
>
> > If sequence spaces cannot be crossed from one point to another, then
> > how does ANY new species form? Why is the crossing of sequence space
> > from point "ape" to point "human" any less likely than the often-much-
> > larger gap from ANY species A to ANY species B?
>
> You need to deal with specific functional systems for which there is
> enough known information to answer such questions. Knowledge of the
> functional aspects of the human and/or ape genomes is not sufficient
> yet.
>
Then, uh, how the hell can you calculate its probability in sequence
space?
> > Other than your religious opinion that humans simply are too divinely
> > "special" to have evolved?
>
> Not at all. Based on what is currently known, a common evolutionary
> ancestor of humans and apes cannot be adequately excluded on a genetic
> basis.
Then what are you bitching about?
'Rev Dr' Lenny Flank
>
> Why do you keep re-posting the same stuff over and over again in the
> very same thread
Because you won't answer.
heekster
wrote:
Putting bullshit and imbecilities on a webpage does not change the
fact that they are bullshit and imbecilities.
Seanpit
> On Dec 1, 11:20 pm, Seanpit <sean...@gmail.com> wrote:
>
> > On 1 Dec, 20:04, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
> > > (snip lots of arm-waving)
>
> > > Hey Sean, if the gap between jaguars and cheetahs isn't too large to
> > > be crossed in sequence space, then why is the much smaller gap between
> > > humans and chimps too large top be crossed in sequence space?
>
> > As I've pointed out to you before, you have no basis to argue that the
> > gap between jaguars and cheetahs is larger than between humans and
> > apes.
>
> Um, humans and chimps are 98.5% identical in their DNA.
Depends on what part of the genome you're looking at. This 98.5%
number is usually based on homologies of protein-coding genes.
However, non-coding functional DNA elements, like miRNA producing
regions of the genome, can be much more different. For example,
miRNAs from the brains of humans and chimps show an overlap of only
83%.
"miRNAs recently have been implicated in synaptic development and
in memory formation. As the species specific miRNAs described here are
expressed in the brain, which is the most complex tissue in the human
body, with an estimated 10,000 different cell types, these miRNAs
could have a role in establishing or maintaining cellular diversity
and could thereby contribute to the differences in human and
chimpanzee brain ... function."
http://www.niob.knaw.nl/researchpages/cuppen/publications/berezikov_NG_human_chimp.pdf
> That is closer than most of the other species which creationists
> assume "microevolved".
It isn't as clear cut as you make it out to be. The functional
differences between humans and apes are not clearly understood on a
genetic level yet.
> So YOU tell ME how YOU measure the genetic gap, then, and by what
> measure "humans" and "chimps" are FURTHER APART than most other
> speices . . . . . . .?
>
> Other than your religious opinion that humans are special and MUST be
> "different" from all other species . . . .
>
> > Jaguars and cheetahs are clearly part of the same genetic pool
> > of options - nothing but Mendelian variations on the same theme.
>
> And since humans and chimps are 98.5% identical in their DNA ---
> closer together than horses and donkeys, or jaguars and cheetahs, they
> too are clearly part of the same genetic pool of options -- nothing
> but Mendelian variations on the same theme.
>
> > In
> > short, they can breed and produce viable and fertile offspring.
> > Humans and apes cannot produce viable much less fertile offspring -
> > indicating significant functional gene pool differences.
>
> So what. Domestic wheat and wild emmer grass can't interbreed and
> produce fertile offspring, yet we know for a historical fact that
> domestic wheat is descended from wild emmer grass.
"Domestic" or "bread wheat" can be crossed with wild emmer wheat and
the F1 hybrid is viable and can be fertile - - 1-2% of the time.
Modern bread wheat varieties have 42 chromosomes and evolved from
crosses between wild emmer, (T. dicoccoides: 28 chromosomes; 4N) and
goat grass (14 chromosomes; 2N). All varieties of wheat grown today
was originally derived from wild 14 chromosome wheat (einkorn). So,
14 is the diploid number (2N) of chromosomes for wheat. Einkorn and
other 14-chromosome (2N) wild grass crosses produced the tetraploid 28
(4N) chromosome wheat.
http://www.answers.com/topic/the-natural-history-of-wheat
"Wild emmer wheat (Triticum dicoccoides Korn, 2n = 4x = 28,
genome AABB) were earlier crossed to two Indian bread wheat (T.
aestivum L., 2n = 6x = 42, genome AABBDD) . . . The germination of F1
seeds and seedling growth up to the 3-4 tiller stage was normal. . .
Crosses were repeated and the partially fertile pentaploid F1 hybrid,
Sonalika x T. dicoccoides was selfed. Two out of eleven F2 segregants
were observed to have spikes similar to that of the F1 hybrid."
http://www.shigen.nig.ac.jp/wheat/wis/No71/p29/1.html
"In direct crosses between the T. dicoccoides selection and the
susceptible T. aestivum cultivars, the pentaploid interspecific
hybrids were highly sterile (fertility of 1–2% by self-pollination);
the F2 population segregated in a 3 resistant:1 susceptible ratio. In
bridge-crosses between the fertile tetraploid progeny of a previous T.
dicoccoides-T. durum cross and susceptible T. aestivum cultivars, the
fertility was markedly improved (approximately 50% when T. aestivum
served as pollinator); the F1 pentaploid hybrids of these three-way
crosses segregated in a pattern fitting a 1 resistant:1 susceptible
ratio."
http://www.springerlink.com/content/v48256521351144m/
Of course, because of differences in genome ploidy, as well as
differences in accumulated recessive alleles in the various "breeds"
of wheat and grass, some of these hybrids will often suffer "hybrid
necrosis, hybrid chlorosis and hybrid dwarfness."
Consider that producing a viable offspring requires that enough
information be present while producing virile offspring requires that
both the genetic information be present as well as the proper
chromosomal structure (see link below).
Again, the fact that humans and apes do not produce viable much less
fertile hybrids while jaguars and cheetahs produce both viable and
fertile offspring is a good clue to the idea that humans and apes are
not as functionally close, genetically speaking, as are jaguars and
cheetahs - or emmer and bread wheat for that matter.
> The grey tree frog
> Hyla chrysoscelis is so identical to the grey tree frog Hyla
> versicolor that they can't be identified in the field, yet they too
> are utterly incapable of producing fertile offspring.
This is another case of ploidy differences. H. versicolor is
tetraploid (4N = 48) while H. chrysoscelis is diploid (2N = 24).
Female H. versicolor frogs that mate with male H. chrysoscelis frogs
produce viable, but sterile offspring - like mules (as a cross between
the horses and donkeys). Sterility is often a problem of chromosomal
arrangement rather than a problem of chromosomal information.
http://www.detectingdesign.com/donkeyshorsesmules.html
Again, compare this with the fact that humans and apes do not produce
viable much less fertile offspring.
> So why is it possible for emmer and wheat, or for H chrysoscelis and H
> versicolor, to cross those "signfiicant functional gene pool
> differences", but not for humans and chimps to do the same?
Your wheat and tree frog examples both produce viable offspring and
your wheat example can even produce fertile offspring. The reason why
the tree frogs in your example produce viable, but sterile, offspring
is likely due to chromosomal structural differences rather than
informational differences. The lack of ability to produce viable
offspring (not just sterile offspring), given the same chromosomal
ploidy number, indicates a significant informational difference
between the two genomes.
> Why is
> it, in your view, that emmer grass can cross the "sequence space" to a
> different species that can't interbreed with it, but chimps could not
> cross the (much closer) "sequence space" to humans?
Emmer grass is not informationally different, qualitatively, from
other forms of wheat or ancestral wheat-like grasses. That is why
crosses between these types of plants can produce viable and even
fertile offspring. This is not the case for human-ape crosses. No
viable offspring much less fertile offspring can be produced.
> Other than your religious assumption that humans are divine and cannot
> have evolved.
That has nothing to do with it.
> > As noted before for you, these differences are likely the result of
> > functional non-coding sequences within the genomes that is often quite
> > different and unique between humans and apes. It seems that
> > functional complexity at such very high levels is based more on non-
> > coding DNA than coding DNA - much much more. Genomic sizes of various
> > creatures reflect this hypothesis with many simpler forms having
> > similar numbers of genes, but far less non-coding DNA (formerly known
> > as 'junk-DNA'). Emergent functional "complexity" therefore seems to be
> > much more closely related to the amount of non-coding DNA vs. coding
> > DNA.
>
> That's nice.
> How is that different in any other species?
>
> Why is nit that OTHER species can cross "sequence space" to new
> species, but only HUMANS can't have crossed the (much smaller)
> "sequence space" between them and apes?
>
> Other than your religious opinion that humans simply can not have
> evolved from anything, period?
I've explained it to you several times now. Humans and apes cannot
produce viable much less fertile offspring while all of the examples
you've listed so far can produce viable offspring. This is likely due
to a significant difference in function information content between
the genomes of humans and apes vs. those crosses that you've just
listed. I've even provided reasonable evidence that suggests that the
primary location of this informational difference is within the non-
coding regions of the genomes.
> > Beyond this, however, not enough information is known as to the actual
> > functional genetic differences between humans and apes.
>
> Then, uh, how the hell can you calculate its probability in sequence
> space?
Based on lower-level sub-cellular systems that we know much more
about. Target ratios are based on specific emergent systems of
function that are known if at least a fair degree of detail. The
functional differences between humans and chimps is not known is
sufficient detail as of yet.
> > > If sequence spaces cannot be crossed from one point to another, then
> > > how does ANY new species form? Why is the crossing of sequence space
> > > from point "ape" to point "human" any less likely than the often-much-
> > > larger gap from ANY species A to ANY species B?
>
> > You need to deal with specific functional systems for which there is
> > enough known information to answer such questions. Knowledge of the
> > functional aspects of the human and/or ape genomes is not sufficient
> > yet.
>
> Then, uh, how the hell can you calculate its probability in sequence
> space?
See above:
> > > Other than your religious opinion that humans simply are too divinely
> > > "special" to have evolved?
>
> > Not at all. Based on what is currently known, a common evolutionary
> > ancestor of humans and apes cannot be adequately excluded on a genetic
> > basis.
>
> Then what are you bitching about?
There are lots of systems and levels of functional complexity that are
known in much more extensive detail that go well beyond the powers of
RM/NS to produce from any other existing system or subsystem within
trillions of years - on average.
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
John Harshman
> On 2 Dec, 05:09, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>> On Dec 1, 11:20 pm, Seanpit <sean...@gmail.com> wrote:
>>
>>> On 1 Dec, 20:04, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>>>> (snip lots of arm-waving)
>>>> Hey Sean, if the gap between jaguars and cheetahs isn't too large to
>>>> be crossed in sequence space, then why is the much smaller gap between
>>>> humans and chimps too large top be crossed in sequence space?
>>> As I've pointed out to you before, you have no basis to argue that the
>>> gap between jaguars and cheetahs is larger than between humans and
>>> apes.
>> Um, humans and chimps are 98.5% identical in their DNA.
>
> Depends on what part of the genome you're looking at. This 98.5%
> number is usually based on homologies of protein-coding genes.
Wrong. It's based on the overall percent identity of all sequences with
homologs present in both species. Since protein-coding (and other
conserved) sequences are a tiny minority of the genome, in effect it's
an assay of junk DNA. Protein-coding sequences are on average 99.5%
identical between species.
> However, non-coding functional DNA elements, like miRNA producing
> regions of the genome, can be much more different. For example,
> miRNAs from the brains of humans and chimps show an overlap of only
> 83%.
What exactly does this mean? Are you talking about the genome or about
expression patterns?
> "miRNAs recently have been implicated in synaptic development and
> in memory formation. As the species specific miRNAs described here are
> expressed in the brain, which is the most complex tissue in the human
> body, with an estimated 10,000 different cell types, these miRNAs
> could have a role in establishing or maintaining cellular diversity
> and could thereby contribute to the differences in human and
> chimpanzee brain ... function."
>
> http://www.niob.knaw.nl/researchpages/cuppen/publications/berezikov_NG_human_chimp.pdf
Ah, it is indeed expression pattern, though they did search the genomes
for recovered sequences. So 83% of candidate miRNAs recovered in this
particular expression study were found in both genomes. Note that many
of these miRNAs are parts of families that have been duplicated, with
divergence, either in human or chimp, so there is a known mechanism
responsible for at least some of the difference. I note also that the
percentage of miRNAs in common between species pairs follows exactly the
pattern expected from phylogeny.
>> That is closer than most of the other species which creationists
>> assume "microevolved".
>
> It isn't as clear cut as you make it out to be. The functional
> differences between humans and apes are not clearly understood on a
> genetic level yet.
Well enough that it seems unlikely there could be any huge neutral gaps
hiding in the genetic differences.
[snip Sean's "baffle with bullshit" phase]
'Rev Dr' Lenny Flank
(snipping lots to make this very long post shorter)
> Depends on what part of the genome you're looking at.
And this differs from other species how, again . . . . ?
By what measure do YOU presume that humans and chimps are further
apart in "sequence space" than, say, jauguars and cheetahs are?
> > That is closer than most of the other species which creationists
> > assume "microevolved".
>
> It isn't as clear cut as you make it out to be.
Yes it is. Until you show some measure indicating that hum ans and
chimps are NOT closer in "sdequence space" than jaguars and cheetahs
are.
Got any?
The functional
> differences between humans and apes are not clearly understood on a
> genetic level yet.
>
Then how the hell do you calculate their "probability"?
> > So YOU tell ME how YOU measure the genetic gap, then, and by what
> > measure "humans" and "chimps" are FURTHER APART than most other
> > speices . . . . . . .?
>
> > Other than your religious opinion that humans are special and MUST be
> > "different" from all other species . . . .
Well . . . . . . . . . . .?
I'm still waiting . . . . . . . . . . .
> > > Jaguars and cheetahs are clearly part of the same genetic pool
> > > of options - nothing but Mendelian variations on the same theme.
>
> > And since humans and chimps are 98.5% identical in their DNA ---
> > closer together than horses and donkeys, or jaguars and cheetahs, they
> > too are clearly part of the same genetic pool of options -- nothing
> > but Mendelian variations on the same theme.
>
Well . . . . . . . ?
> > > In
> > > short, they can breed and produce viable and fertile offspring.
> > > Humans and apes cannot produce viable much less fertile offspring -
> > > indicating significant functional gene pool differences.
>
> > So what. Domestic wheat and wild emmer grass can't interbreed and
> > produce fertile offspring, yet we know for a historical fact that
> > domestic wheat is descended from wild emmer grass.
>
> "Domestic" or "bread wheat" can be crossed with wild emmer wheat and
> the F1 hybrid is viable and can be fertile - - 1-2% of the time.
Great. Glad to hear it.
So what? Does that make them the same "kind"? Does it make them
closer in "sequence space" than humans and chimps? How can you tell?
>
> Modern bread wheat varieties have 42 chromosomes and evolved from
> crosses between wild emmer, (T. dicoccoides: 28 chromosomes; 4N) and
> goat grass (14 chromosomes; 2N). All varieties of wheat grown today
> was originally derived from wild 14 chromosome wheat (einkorn). So,
> 14 is the diploid number (2N) of chromosomes for wheat. Einkorn and
> other 14-chromosome (2N) wild grass crosses produced the tetraploid 28
> (4N) chromosome wheat.
>
> http://www.answers.com/topic/the-natural-history-of-wheat
OK, so you can accurately cut and paste from a website. My nine year
old nephew can do that too.
Now answer my goddamn question. If other speices can evolve from one
point in "sequence space" to another, then why can't humans evolve
from the much-genetically-closer ape point in sequence space?
Other than your religious wish that it not be so.
> Again, the fact that humans and apes do not produce viable much less
> fertile hybrids while jaguars and cheetahs produce both viable and
> fertile offspring is a good clue to the idea that humans and apes are
> not as functionally close, genetically speaking, as are jaguars and
> cheetahs - or emmer and bread wheat for that matter.
By what measure.
>
> > The grey tree frog
> > Hyla chrysoscelis is so identical to the grey tree frog Hyla
> > versicolor that they can't be identified in the field, yet they too
> > are utterly incapable of producing fertile offspring.
>
> This is another case of ploidy differences.
No shit.
H. versicolor is
> tetraploid (4N = 48) while H. chrysoscelis is diploid (2N = 24).
> Female H. versicolor frogs that mate with male H. chrysoscelis frogs
> produce viable, but sterile offspring - like mules (as a cross between
> the horses and donkeys). Sterility is often a problem of chromosomal
> arrangement rather than a problem of chromosomal information.
No shit.
So what?
>
> http://www.detectingdesign.com/donkeyshorsesmules.html
>
> Again, compare this with the fact that humans and apes do not produce
> viable much less fertile offspring.
Says you. (shrug)
But you've still not answered my question. If species A can evolve to
species B by crossing your "sequence space", then why can't apes
evolve into humans by crossing a much smaller space?
The lack of ability to produce viable
> offspring (not just sterile offspring), given the same chromosomal
> ploidy number, indicates a significant informational difference
> between the two genomes.
That's nice.
And that has what, again, to do with your "sequence space"?
Is it therefore your opinion that any genetic change which leads to
infertility, is an "informational difference betwen the two genomes"
that is too great to cross?
If so, then, uh, how do ANY new species form . . . .?
>
> > Why is
> > it, in your view, that emmer grass can cross the "sequence space" to a
> > different species that can't interbreed with it, but chimps could not
> > cross the (much closer) "sequence space" to humans?
>
> Emmer grass is not informationally different, qualitatively, from
> other forms of wheat or ancestral wheat-like grasses.
By what measure?
And by what measure do you presume that humans and chimps are
"informationally different" (whatever the hell THAT means),
qualitavely, from each other or other apes?
> > Other than your religious assumption that humans are divine and cannot
> > have evolved.
>
> That has nothing to do with it.
Don't bullshit me, Sean.
Seanpit
wrote:
>
> >> Um, humans and chimps are 98.5% identical in their DNA.
>
> > Depends on what part of the genome you're looking at. This 98.5%
> > number is usually based on homologies of protein-coding genes.
>
> Wrong. It's based on the overall percent identity of all sequences with
> homologs present in both species. Since protein-coding (and other
> conserved) sequences are a tiny minority of the genome, in effect it's
> an assay of junk DNA. Protein-coding sequences are on average 99.5%
> identical between species.
Most estimates of sequence divergence have focused exclusively on base
substitutions in DNA—that is, one base (or one DNA ‘letter’—A, T, C or
G) being replaced with another. More recent calculations also include
insertions and deletions, or indels, in addition to base
substitutions. The author of one such study, Roy J. Britten, argues:
"It appears appropriate to me to consider the full length of the
gaps in estimating the interspecies divergence. These stretches of DNA
are actually absent from one and present in the other genome. In the
past, indels have often simply been counted regardless of length and
added to the base substitution count, because that is convenient for
phylogenetics."
Britten, R.J., Divergence between samples of chimpanzee and human DNA
sequences is 5%, counting indels, Proc. Nat. Acad. Sci. USA 99(21):
13633–13635, 2002.
His findings lend support to the idea that much of the failure of DNA
to hybridize between chimps and humans is the result of missing DNA
due to indel events.
Britten then became involved in a follow-up paper in which these
initial results were confirmed; in fact, it was found that "the 5%
human-chimp difference already published is likely to be an
underestimate, possibly by more than a factor of 2." - - in other
words by more than 10%.
Britten, R.J., Rowen, L., Williams, J. and Cameron, R.A., Majority of
divergence between closely related DNA samples is due to indels, Proc.
Nat. Acad. Sci. USA 100(8):4661–4665, 2003.
Then, Anzai et al. published a study where nearly one-half of the MHC
region was sequenced - within chimps. The sequence results in
comparison the the human region actually dropped the DNA similarity
estimate down to 86.7%. Anzai concluded that the 86.7% estimate "may
be a better representation of whole-genome sequence similarity between
the human and the chimpanzee" than previous estimates of 98.6% since
"the major difference between the human and chimpanzee sequences is
overwhelmingly attributable to indels".
Anzai, T., Shiina, T., Kimura, N., Yanagiya, K., Kohara, S.,
Shigenari, A., Yamagata, T., Kulski, J.K., Naruse, T.K., Fujimori, Y.,
Fukuzumi, Y., Yamazaki, M., Tashiro, H., Iawmoto, C., Umehara, Y.,
Imanishi, T., Meyer, A., Ikeo, K., Gojobori, T., Bahram, S. and Inoko,
H., Comparative sequencing of human and chimpanzee MHC class I regions
unveils insertions/deletions as the major path to genomic divergence,
Proc. Nat. Acad. Sci. USA 100(13):7708–7713, 2003.
Of course, other studies, have resulted in estimates of similarity
higher than 98.6%. For instance, Wildman et al.compared ~90 kilobases
of human DNA to chimps and found a similarity of 98.86%, even when
counting indels.
Wildman, D.E., Uddin, M., Liu, G., Grossman, L.I. and Goodman, M.,
Implications of natural selection in shaping 99.4% nonsynonymous DNA
identity between humans and chimpanzees: enlarging genus Homo, Proc.
Nat. Acad. Sci. USA 100(12):7181–7188, 2003.
This seems to be in direct opposition to the data presented by Britten
and Anzai et al. However, Wildman’s team examined only coding DNA from
a number of genes. Britten and Anzai both considered non-coding DNA in
their studies and therefore consider a greater range of DNA types in
their conclusion of an 86.7 similarity.
See also:
http://www.answersingenesis.org/tj/v18/i2/similarity.asp
> > However, non-coding functional DNA elements, like miRNA producing
> > regions of the genome, can be much more different. For example,
> > miRNAs from the brains of humans and chimps show an overlap of only
> > 83%.
>
> What exactly does this mean? Are you talking about the genome or about
> expression patterns?
Both . . .
> > "miRNAs recently have been implicated in synaptic development and
> > in memory formation. As the species specific miRNAs described here are
> > expressed in the brain, which is the most complex tissue in the human
> > body, with an estimated 10,000 different cell types, these miRNAs
> > could have a role in establishing or maintaining cellular diversity
> > and could thereby contribute to the differences in human and
> > chimpanzee brain ... function."
>
> >http://www.niob.knaw.nl/researchpages/cuppen/publications/berezikov_N...
>
> Ah, it is indeed expression pattern, though they did search the genomes
> for recovered sequences. So 83% of candidate miRNAs recovered in this
> particular expression study were found in both genomes. Note that many
> of these miRNAs are parts of families that have been duplicated, with
> divergence, either in human or chimp, so there is a known mechanism
> responsible for at least some of the difference. I note also that the
> percentage of miRNAs in common between species pairs follows exactly the
> pattern expected from phylogeny.
All bets are off when NS is involved as a preserving force over
time. Here we have 17% miRNAs that are not homologous between species
- and that is just one type of non-coding potentially functional DNA
type. This isn't just an expression pattern. This represents unique
genomic differences that are likely functionally important.
> >> That is closer than most of the other species which creationists
> >> assume "microevolved".
>
> > It isn't as clear cut as you make it out to be. The functional
> > differences between humans and apes are not clearly understood on a
> > genetic level yet.
>
> Well enough that it seems unlikely there could be any huge neutral gaps
> hiding in the genetic differences.
You can't say that unless you actually know something about the end-
product functional differences - differences that may be and are
likely the result of many miRNAs and other non-coding elements using
similar gene-product building blocks to build functionally novel
systems. This is in fact suggested to be the reason for structural
and functional differences between the brains of humans and chimps.
> [snip Sean's "baffle with bullshit" phase]
What? You think the fact that humans and apes do not produce viable
much less fertile offspring is irrelevant? How is the presentation of
examples of interbreeding species that produce at least viable and
even occasionally fertile offspring at all germane when it comes to
the argument that humans and chimps are even more closely related? -
even though they cannot produce viable much less fertile offspring?
Who's BSing here?
Sean Pitman
www.DetectingDesign.com
Mark Isaak
> [new DNA sequence appears]
> Not necessarily. It just is unlikely to hit upon a new type of
> function, a function that was not already in the genome pool to begin
> with, that requires at least 600aa at minimum to work.
How unlikely?
To specific in my question: Suppose I give you a 600aa sequence, built by
randomly selecting each site from available amino acids. What is the
probability of it being functional? I am looking for the number and an
explanation of how it was derived.
--
Mark Isaak eciton (at) earthlink (dot) net
"Voice or no voice, the people can always be brought to the bidding of
the leaders. That is easy. All you have to do is tell them they are
being attacked, and denounce the pacifists for lack of patriotism and
exposing the country to danger." -- Hermann Goering
John Harshman
> On 2 Dec, 15:58, John Harshman <jharshman.diespam...@pacbell.net>
> wrote:
>>>> Um, humans and chimps are 98.5% identical in their DNA.
>>> Depends on what part of the genome you're looking at. This 98.5%
>>> number is usually based on homologies of protein-coding genes.
>> Wrong. It's based on the overall percent identity of all sequences with
>> homologs present in both species. Since protein-coding (and other
>> conserved) sequences are a tiny minority of the genome, in effect it's
>> an assay of junk DNA. Protein-coding sequences are on average 99.5%
>> identical between species.
>
> Most estimates of sequence divergence have focused exclusively on base
> substitutions in DNA—that is, one base (or one DNA ‘letter’—A, T, C or
> G) being replaced with another. More recent calculations also include
> insertions and deletions, or indels, in addition to base
> substitutions.
No, those aren't more recent calculations. They're just different. None
of the numbers you have quoted have anything to do with counting indels.
What follows here is more of your "baffling with bullshit" tactic. When
you're wrong, you just cite irrelevant studies.
> The author of one such study, Roy J. Britten, argues:
>
> "It appears appropriate to me to consider the full length of the
> gaps in estimating the interspecies divergence. These stretches of DNA
> are actually absent from one and present in the other genome. In the
> past, indels have often simply been counted regardless of length and
> added to the base substitution count, because that is convenient for
> phylogenetics."
Yes, and I think Britten's idea is silly. What biological reason is
there to count the lengths of gaps, when each gap is generally a single
mutation? A 1-base gap is 1 mutation; a thousand-base gap is 1 mutation.
> Britten, R.J., Divergence between samples of chimpanzee and human DNA
> sequences is 5%, counting indels, Proc. Nat. Acad. Sci. USA 99(21):
> 13633–13635, 2002.
>
> His findings lend support to the idea that much of the failure of DNA
> to hybridize between chimps and humans is the result of missing DNA
> due to indel events.
What failure to hybridize are you talking about here? Perhaps you mean
that most sequences that don't hybridize are those that are not shared.
That makes sense, as the other reason for having a non-hybridized
fraction in a DNA-DNA hybridization experiment is high sequence
divergence, which isn't going to happen between humans and chimps.
> Britten then became involved in a follow-up paper in which these
> initial results were confirmed; in fact, it was found that "the 5%
> human-chimp difference already published is likely to be an
> underestimate, possibly by more than a factor of 2." - - in other
> words by more than 10%.
Again, the estimate is biologically meaningless.
> Britten, R.J., Rowen, L., Williams, J. and Cameron, R.A., Majority of
> divergence between closely related DNA samples is due to indels, Proc.
> Nat. Acad. Sci. USA 100(8):4661–4665, 2003.
>
> Then, Anzai et al. published a study where nearly one-half of the MHC
> region was sequenced - within chimps. The sequence results in
> comparison the the human region actually dropped the DNA similarity
> estimate down to 86.7%. Anzai concluded that the 86.7% estimate "may
> be a better representation of whole-genome sequence similarity between
> the human and the chimpanzee" than previous estimates of 98.6% since
> "the major difference between the human and chimpanzee sequences is
> overwhelmingly attributable to indels".
Once again, biologically meaningless.
> Anzai, T., Shiina, T., Kimura, N., Yanagiya, K., Kohara, S.,
> Shigenari, A., Yamagata, T., Kulski, J.K., Naruse, T.K., Fujimori, Y.,
> Fukuzumi, Y., Yamazaki, M., Tashiro, H., Iawmoto, C., Umehara, Y.,
> Imanishi, T., Meyer, A., Ikeo, K., Gojobori, T., Bahram, S. and Inoko,
> H., Comparative sequencing of human and chimpanzee MHC class I regions
> unveils insertions/deletions as the major path to genomic divergence,
> Proc. Nat. Acad. Sci. USA 100(13):7708–7713, 2003.
>
> Of course, other studies, have resulted in estimates of similarity
> higher than 98.6%. For instance, Wildman et al.compared ~90 kilobases
> of human DNA to chimps and found a similarity of 98.86%, even when
> counting indels.
>
> Wildman, D.E., Uddin, M., Liu, G., Grossman, L.I. and Goodman, M.,
> Implications of natural selection in shaping 99.4% nonsynonymous DNA
> identity between humans and chimpanzees: enlarging genus Homo, Proc.
> Nat. Acad. Sci. USA 100(12):7181–7188, 2003.
>
> This seems to be in direct opposition to the data presented by Britten
> and Anzai et al. However, Wildman’s team examined only coding DNA from
> a number of genes. Britten and Anzai both considered non-coding DNA in
> their studies and therefore consider a greater range of DNA types in
> their conclusion of an 86.7 similarity.
Blah, blah. More irrelevant nonsense, except that you provide a quote
for my statement that protein-coding regions average 99.5% identity.
> See also:
> http://www.answersingenesis.org/tj/v18/i2/similarity.asp
>
>>> However, non-coding functional DNA elements, like miRNA producing
>>> regions of the genome, can be much more different. For example,
>>> miRNAs from the brains of humans and chimps show an overlap of only
>>> 83%.
>> What exactly does this mean? Are you talking about the genome or about
>> expression patterns?
>
> Both . . .
Not good. You need to untangle them if you want to know what's happening.
>>> "miRNAs recently have been implicated in synaptic development and
>>> in memory formation. As the species specific miRNAs described here are
>>> expressed in the brain, which is the most complex tissue in the human
>>> body, with an estimated 10,000 different cell types, these miRNAs
>>> could have a role in establishing or maintaining cellular diversity
>>> and could thereby contribute to the differences in human and
>>> chimpanzee brain ... function."
>>> http://www.niob.knaw.nl/researchpages/cuppen/publications/berezikov_N...
>> Ah, it is indeed expression pattern, though they did search the genomes
>> for recovered sequences. So 83% of candidate miRNAs recovered in this
>> particular expression study were found in both genomes. Note that many
>> of these miRNAs are parts of families that have been duplicated, with
>> divergence, either in human or chimp, so there is a known mechanism
>> responsible for at least some of the difference. I note also that the
>> percentage of miRNAs in common between species pairs follows exactly the
>> pattern expected from phylogeny.
>
> All bets are off when NS is involved as a preserving force over
> time. Here we have 17% miRNAs that are not homologous between species
> - and that is just one type of non-coding potentially functional DNA
> type. This isn't just an expression pattern. This represents unique
> genomic differences that are likely functionally important.
Again, it's 17% of the candidate miRNAs that were recovered in a
particular expression study that are not *orthologous* to one in the
other species.
>>>> That is closer than most of the other species which creationists
>>>> assume "microevolved".
>>> It isn't as clear cut as you make it out to be. The functional
>>> differences between humans and apes are not clearly understood on a
>>> genetic level yet.
>> Well enough that it seems unlikely there could be any huge neutral gaps
>> hiding in the genetic differences.
>
> You can't say that unless you actually know something about the end-
> product functional differences - differences that may be and are
> likely the result of many miRNAs and other non-coding elements using
> similar gene-product building blocks to build functionally novel
> systems. This is in fact suggested to be the reason for structural
> and functional differences between the brains of humans and chimps.
And it may be part of the reason. But miRNAs are short and can easily
evolve. We also have no data suggesting that any of this requires
crossing of any large, neutral gap, and every reason to believe that
individual mutations could be selectively advantageous.
>> [snip Sean's "baffle with bullshit" phase]
>
> What? You think the fact that humans and apes do not produce viable
> much less fertile offspring is irrelevant?
Yes. Some closely related species can't produce viable offspring. Some
distantly related species can. There is no particular correlation
between closeness of relationship and hybridization.
> How is the presentation of
> examples of interbreeding species that produce at least viable and
> even occasionally fertile offspring at all germane when it comes to
> the argument that humans and chimps are even more closely related?
It isn't. Nor is the inability of chimps and humans to hybridize.
> even though they cannot produce viable much less fertile offspring?
> Who's BSing here?
You are, as I've already mentioned several times.
Seanpit
< snip >
> > > > In
> > > > short, they can breed and produce viable and fertile offspring.
> > > > Humans and apes cannot produce viable much less fertile offspring -
> > > > indicating significant functional gene pool differences.
>
> > > So what. Domestic wheat and wild emmer grass can't interbreed and
> > > produce fertile offspring, yet we know for a historical fact that
> > > domestic wheat is descended from wild emmer grass.
>
> > "Domestic" or "bread wheat" can be crossed with wild emmer wheat and
> > the F1 hybrid is viable and can be fertile - - 1-2% of the time.
>
> Great. Glad to hear it.
>
> So what? Does that make them the same "kind"? Does it make them
> closer in "sequence space" than humans and chimps? How can you tell?
Yes, it does. The ability to produce viable offspring (not fertile
mind you; just viable) means that the essentially the same information
is present (qualitatively) in both of the mating individuals. Nothing
is missing as far as qualitative information or else a viable embryo
could not be produced.
Fertility isn't an informational problem as much as it is a
chromosomal structural problem. Again, read the link I gave you on
the reason why mules are almost always sterile - it isn't because of
lack of genetic information.
> > Modern bread wheat varieties have 42 chromosomes and evolved from
> > crosses between wild emmer, (T. dicoccoides: 28 chromosomes; 4N) and
> > goat grass (14 chromosomes; 2N). All varieties of wheat grown today
> > was originally derived from wild 14 chromosome wheat (einkorn). So,
> > 14 is the diploid number (2N) of chromosomes for wheat. Einkorn and
> > other 14-chromosome (2N) wild grass crosses produced the tetraploid 28
> > (4N) chromosome wheat.
>
> >http://www.answers.com/topic/the-natural-history-of-wheat
>
> OK, so you can accurately cut and paste from a website. My nine year
> old nephew can do that too.
>
> Now answer my goddamn question. If other speices can evolve from one
> point in "sequence space" to another, then why can't humans evolve
> from the much-genetically-closer ape point in sequence space?
Although it can't be adequately supported at this point due to a lack
of knowledge, the available evidence suggests that humans and chimps
are actually farther apart in sequence space than all of the other
species pairs that you've presented so far - because of the simple
fact that all of your examples produce viable and even virile
offspring while the human-chimp combo does not produce any viable much
less virile offspring.
> Other than your religious wish that it not be so.
Seems to me like your religion is blinding you just a bit here to the
obvious here.
> > Again, the fact that humans and apes do not produce viable much less
> > fertile hybrids while jaguars and cheetahs produce both viable and
> > fertile offspring is a good clue to the idea that humans and apes are
> > not as functionally close, genetically speaking, as are jaguars and
> > cheetahs - or emmer and bread wheat for that matter.
>
> By what measure.
The measure is not adequately determinable except to say that the
human-chimp distance is likely greater, by some unknown measure,
compared to emmer and bread wheat or jaguars and cheetahs.
> > > The grey tree frog
> > > Hyla chrysoscelis is so identical to the grey tree frog Hyla
> > > versicolor that they can't be identified in the field, yet they too
> > > are utterly incapable of producing fertile offspring.
>
> > This is another case of ploidy differences.
>
> No shit.
>
> > H. versicolor is
> > tetraploid (4N = 48) while H. chrysoscelis is diploid (2N = 24).
> > Female H. versicolor frogs that mate with male H. chrysoscelis frogs
> > produce viable, but sterile offspring - like mules (as a cross between
> > the horses and donkeys). Sterility is often a problem of chromosomal
> > arrangement rather than a problem of chromosomal information.
>
> No shit.
>
> So what?
So what? That's what the non-beneficial gap problem is all about -
novel functional informational differences (qualitative differences).
> >http://www.detectingdesign.com/donkeyshorsesmules.html
>
> > Again, compare this with the fact that humans and apes do not produce
> > viable much less fertile offspring.
>
> Says you. (shrug)
There have been actual studies . . .
> But you've still not answered my question. If species A can evolve to
> species B by crossing your "sequence space", then why can't apes
> evolve into humans by crossing a much smaller space?
The likely space is larger, not smaller, than your examples. I'm not
sure how much larger or if the gap is too large to have been crossed
by RM/NS because we do not yet know enough to make such a
determination to an adequate level of confidence.
> > The lack of ability to produce viable
> > offspring (not just sterile offspring), given the same chromosomal
> > ploidy number, indicates a significant informational difference
> > between the two genomes.
>
> That's nice.
>
> And that has what, again, to do with your "sequence space"?
Again, targets within sequence space are defined by novel functionally
beneficial differences from what already exists within a given
genome.
> Is it therefore your opinion that any genetic change which leads to
> infertility, is an "informational difference betwen the two genomes"
> that is too great to cross?
No. What I'm saying is that two species that cannot produce viable
much less fertile offspring are likely to be farther apart in sequence
space, on different functional islands at a given level, compared to
those creatures than can produce viable offspring and certain compared
to those creatures that can produce both viable and fertile
offspring.
> If so, then, uh, how do ANY new species form . . . .?
The term "species" is a very subjective term that is very difficult to
definitively define in a scientific manner. The real question is, how
are novel functional elements added into a genome pool of options?
For low-level systems that require no more than a few hundred fsaars
at minimum the mechanism of RM/NS does the job just fine. However,
when it comes to systems beyond the 1000 fsaar level of functional
complexity, only the input of at least human-level intelligence and
technology is known to be able to do the job. No known non-
intelligent force of nature comes remotely close.
> > > Why is
> > > it, in your view, that emmer grass can cross the "sequence space" to a
> > > different species that can't interbreed with it, but chimps could not
> > > cross the (much closer) "sequence space" to humans?
>
> > Emmer grass is not informationally different, qualitatively, from
> > other forms of wheat or ancestral wheat-like grasses.
>
> By what measure?
By any measure. There is no qualitative difference, genetically,
between emmer wheat and bread wheat. The only differences are
quantitative. That not the evolution of novel functional differences
within a gene pool of options. Such differences are largely the
result of Mendelian-type variation within an otherwise static gene
pool of options.
> And by what measure do you presume that humans and chimps are
> "informationally different" (whatever the hell THAT means),
> qualitavely, from each other or other apes?
I just told you - the actual degree is not known at this point. The
only thing that the data suggests is that whatever the degree actually
is, it is likely much greater, qualitatively, than any of the examples
you've presented so far.
> > > Other than your religious assumption that humans are divine and cannot
> > > have evolved.
>
> > That has nothing to do with it.
>
> Don't bullshit me, Sean.
Ditto . . .
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
Seanpit
> On Mon, 1 Dec 2008 19:56:59 -0800 (PST), Seanpit <sean...@gmail.com>
Great - please detail exactly where I went wrong in my thinking . . .
This should be good coming from someone who thinks the photos of the
"monuments" in Monument Valley presented on my website are "lava
plugs" rather than sedimentary layers. ; )
__________
> Sean Pitman:
> Care to specifically point out where I misidentify lava plugs are
>"sedimentary"? Please do quote me directly here . . .
Heekster:
"Places like Monument Valley also pose a significant problem. In this
valley, there are formations sticking out of the ground in the middle
of nowhere. These are sedimentary formations that match the Geologic
Column, and yet all around them the rest of the column has vanished.
These formations are made up of horizontal layers that match each
other. Obviously the layers that make up these monuments were once
connected before these intervening sediments were eroded away. "
The picture: http://www.detectingdesign.com/images/Geology/GC_12.jpg
_____
Will you even recognize an error as blatant as this one? I doubt
it . . .
Sean Pitman
www.DetectingDesign.com
'Rev Dr' Lenny Flank
> On 2 Dec, 17:02, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
> < snip >
>
>
>
>
>
> > > > > In
> > > > > short, they can breed and produce viable and fertile offspring.
> > > > > Humans and apes cannot produce viable much less fertile offspring -
> > > > > indicating significant functional gene pool differences.
>
> > > > So what. Domestic wheat and wild emmer grass can't interbreed and
> > > > produce fertile offspring, yet we know for a historical fact that
> > > > domestic wheat is descended from wild emmer grass.
>
> > > "Domestic" or "bread wheat" can be crossed with wild emmer wheat and
> > > the F1 hybrid is viable and can be fertile - - 1-2% of the time.
>
> > Great. Glad to hear it.
>
> > So what? Does that make them the same "kind"? Does it make them
> > closer in "sequence space" than humans and chimps? How can you tell?
>
> Yes, it does. The ability to produce viable offspring (not fertile
> mind you; just viable) means that the essentially the same information
> is present (qualitatively) in both of the mating individuals. Nothing
> is missing as far as qualitative information or else a viable embryo
> could not be produced.
Says you. (shrug)
It is of course entirely possible for two speices to have eaxtly the
same genes, nucleotide for nculeotide, and yet if one of them has a
large inverted section in a critical area, they won't be able to
produce viable offspring. So your entire assumption (interfertility
equals identity of "genetic information") is just a BS assumption on
yourn part that you can't demonstrate in any way whatsoever.
You've still not answered the most basic elementary of questions: How
do you measure this "distance in sequence space", and how can you
therefore show that humans and chimps are further apart in it than any
other two species are.
> Fertility isn't an informational problem as much as it is a
> chromosomal structural problem. Again, read the link I gave you on
> the reason why mules are almost always sterile - it isn't because of
> lack of genetic information.
Measured in what way.
How many units of "genetic information" do humans and chimps differ
by, and how many units of "genetic information" do cheetahs and
jaguars difer by.
> > Now answer my goddamn question. If other speices can evolve from one
> > point in "sequence space" to another, then why can't humans evolve
> > from the much-genetically-closer ape point in sequence space?
>
> Although it can't be adequately supported at this point due to a lack
> of knowledge
Then HOW THE HELL CAN YOU CALCULATE ITS PROBABILITY ????????
, the available evidence suggests that humans and chimps
> are actually farther apart in sequence space than all of the other
> species pairs that you've presented so far
How can we tell.
What units do we measure "farther apart in sequence space" with, and
how can you show me with whatever units and methods you use to measure
it, that chimps/humans are farther apart than, say, cheetahs/jaguars.
I don't want your assumptions and arm-waving. I want some actual live
measurements. That will settle the wholoe question, quuickly, easily
and unmistakably, without any need for arm-waving on your part.
Either the human/chimp "gap in sequewnce space" is bigger, or it's
not. Period. End of debate. All we need is a simple measurement.
Got any?
- because of the simple
> fact that all of your examples produce viable and even virile
> offspring while the human-chimp combo does not produce any viable much
> less virile offspring.
Says you. (shrug)
>
> > Other than your religious wish that it not be so.
>
> Seems to me like your religion is blinding you just a bit here to the
> obvious here.
Nice evasion.
Just as an aside, if you are assuming I am an atheist, you are quite
mistaken.
> > > Again, the fact that humans and apes do not produce viable much less
> > > fertile hybrids while jaguars and cheetahs produce both viable and
> > > fertile offspring is a good clue to the idea that humans and apes are
> > > not as functionally close, genetically speaking, as are jaguars and
> > > cheetahs - or emmer and bread wheat for that matter.
>
> > By what measure.
>
> The measure is not adequately determinable
THEN WHAT THE FUCK ARE YOU GIBBERING ABOUT ???????????????
Dammmmmnnnnnn........
How the hell can you say chimps and humans are "farther apart in
sequence space than this or that other species" if you DON'T EVEN KNOW
HOW TO MEASURE THE GODDAMN DISTANCE???????????
>except to say that the
> human-chimp distance is likely greater, by some unknown measure,
What the hell does THIS even mean?
You're blithering again, Sean.
I say that the chimp/human distance is likely CLOSER, by some unknown
measure. And I can back that up by ppointing out that humans/chimps
are 98.5% identical in their DNA --- a closer percentage than most
other pairs of species.
So there.
Show me why I am wrong. And try to do it with something other than
"an unknown measure".
> So what? That's what the non-beneficial gap problem is all about -
> novel functional informational differences (qualitative differences).
So what, again? You can't even tell me how to MEASURE this "gap",
much less know if the human/chimp "gap" is "larger in sequence space"
than any other. So you are, with all duer respect, just talking out
your ass. (shrug)
And what the hell is a "novel functional informational difference"?
How the hell do you measure THAT?
Wait wait, let me guess --- it's an "unknown measurement" too, but
you're still absolutely certain it shows that humans arenb't related
to chimps. Right . . . . ?
>
> > > Again, compare this with the fact that humans and apes do not produce
> > > viable much less fertile offspring.
>
> > Says you. (shrug)
>
> There have been actual studies . . .
For example . . . . . ?
>
> > But you've still not answered my question. If species A can evolve to
> > species B by crossing your "sequence space", then why can't apes
> > evolve into humans by crossing a much smaller space?
>
> The likely space is larger, not smaller, than your examples.
Says who, and how can we tell?
Show me the measurements.
Humans and chimps are 98.5% identical, genetically.
How close are jaguars and cheetahs?
I'm not
> sure how much larger or if the gap is too large to have been crossed
> by RM/NS because we do not yet know enough to make such a
> determination to an adequate level of confidence.
And because you don't have the foggiest damn idea how to measure this
"gap", and don't have a clue if it's bigger or smaller than any other
"gap". (shrug)
Other than your religious assumption that it MUST be so, by some, uh,
"unknown measurement".
>
> > > The lack of ability to produce viable
> > > offspring (not just sterile offspring), given the same chromosomal
> > > ploidy number, indicates a significant informational difference
> > > between the two genomes.
>
> > That's nice.
>
> > And that has what, again, to do with your "sequence space"?
>
> Again, targets within sequence space are defined by novel functionally
> beneficial differences
And what the hell is THAT, exactly . . . ?
>from what already exists within a given
> genome.
>
And how do we measure that, again? Ohhhh, you don't have the faintest
damn idea, do you . . . . .
Do you wonder why nobody takes you seriously, Sean?
> > Is it therefore your opinion that any genetic change which leads to
> > infertility, is an "informational difference betwen the two genomes"
> > that is too great to cross?
>
> No. What I'm saying is that two species that cannot produce viable
> much less fertile offspring are likely to be farther apart in sequence
> space, on different functional islands at a given level, compared to
> those creatures than can produce viable offspring and certain compared
> to those creatures that can produce both viable and fertile
> offspring.
And we measure that how, again . . . . .?
I say that two species that share 98.5% of their DNA, are likely to be
CLOSER in sequence space than two species with larger differences in
their DNA.
How can we tell which of us is correct? How do you propose we measure
your, uh, "gap in sequence space"? What units do you propose we use?
Or are we to simply assume, as you do, that humans MUST be further
from all other animals "by some unknown measurement", simply because
your religious beleifs tell you that it's so?
>
> > If so, then, uh, how do ANY new species form . . . .?
>
> The term "species" is a very subjective term that is very difficult to
> definitively define in a scientific manner.
Let's use the definition "a set of populkations that share a common
gene pool in the wild".
So I'll ask again --- how do ANY new species form?
The real question is, how
> are novel functional elements added into a genome pool of options?
No, the real question is (1) what the hell is a "novel functional
element", and (2) how do we measure its distance in "sequence space"?
Until you can answer either of those, you are just waving your arms
and blowing smoke. (shrug)
> For low-level systems that require no more than a few hundred fsaars
> at minimum the mechanism of RM/NS does the job just fine. However,
> when it comes to systems beyond the 1000 fsaar level of functional
> complexity, only the input of at least human-level intelligence and
> technology is known to be able to do the job. No known non-
> intelligent force of nature comes remotely close.
Says you. (shrug)
Let me know when you can produce some measurements and show me some
numbers. Until then, all we have is your holy word for it. And your
holy word simply doesn't impress me all that much. Particularly since
your entire argument is just a big long wordy version of the same old
"no new genetic information can appear" horse shit that we've heard
from creation "scientists" for over 40 years now (except that you've
added the fancy scientific-sounding phrase "gap in sequence space",
which you can't measure or even define, anyway).
Nothing new from you, Sean. Same ole same ole.
No WONDER creationism is dead as a mackerel. (shrug)
wf3h
> On 2 Dec, 17:02, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
> >
> > If so, then, uh, how do ANY new species form . . . .?
>
> The term "species" is a very subjective term that is very difficult to
> definitively define in a scientific manner. The real question is, how
> are novel functional elements added into a genome pool of options?
> For low-level systems that require no more than a few hundred fsaars
> at minimum the mechanism of RM/NS does the job just fine. However,
> when it comes to systems beyond the 1000 fsaar level of functional
> complexity, only the input of at least human-level intelligence and
> technology is known to be able to do the job. No known non-
> intelligent force of nature comes remotely close.
what sean ignores, however, is that, if evolution is wrong, then NO
processes are known which can cause speciation. and that includes
intelligent processes, especially since there are no intelligent
processes in nature. none.
the attempt to explain 'natural processes' by 'intelligent design' has
failed for thousands of years. sean has no statistics to back up his
claim that his has happened, nor has he produced the stats to show
that natural processes are impossible.
the failure of sean to present ANY data in support of his position,
coupled with his unsupported assertions that natural processes can be
ruled out lead to the conclusion that he's arguing for a religious,
not a scientific position
'Rev Dr' Lenny Flank
>
> Great - please detail exactly where I went wrong in my thinking . . .
What "thinking"? All I've seen from you is "there's no current
genetic reason to say that humans and chimps are not related by
descent, but I think they are because of a, uh, unknown measurement
that I can't describe or measure."
BFD.
Why don't you just post some quotes from Henry Morris declaring that
"new genetic information can't appear randomly". That's shorter to
say, easier to remember, and was already demonstrated to be bullshit
twenty years ago, so it saves everybody's time. (shrug)
wf3h
>>
> It is of course entirely possible for two speices to have eaxtly the
> same genes, nucleotide for nculeotide, and yet if one of them has a
> large inverted section in a critical area, they won't be able to
> produce viable offspring. So your entire assumption (interfertility
> equals identity of "genetic information") is just a BS assumption on
> yourn part that you can't demonstrate in any way whatsoever.
>
> You've still not answered the most basic elementary of questions: How
> do you measure this "distance in sequence space", and how can you
> therefore show that humans and chimps are further apart in it than any
> other two species are.
for sean to tell you this will require that you provide him with
-your mother's maiden name
-your bank acct number
-your SSN
-your blood type
-your 3rd girlfriend's great grandmother's middle name
and any other irrelevant questions he can come up with
>
> Let me know when you can produce some measurements and show me some
> numbers. Until then, all we have is your holy word for it.
that's pretty much his whole argument. he says that evolution is
impossible. how does he know this? well...he wouldn't say it if it
weren't true. how does he know creationism is true? again, he wouldn't
say it if it weren't true
he keeps getting these responses: requests for data on his assertions;
proof that his view of creationism has statistical support. and he
refuses to say anything at all beyond 'god did it'
'Rev Dr' Lenny Flank
Such differences are largely the
> result of Mendelian-type variation within an otherwise static gene
> pool of options.
>
Would a descendent species that has a single chromosome produced by
the fusion of two different chromosomes in its ancestor, count, in
your view, as a "Mendelian-type variation within an otherwise static
gene pool of options"?
Even if it meant that the two species could no longer produce viable
zygotes?
Why nor why not?
'Rev Dr' Lenny Flank
> the failure of sean to present ANY data in support of his position,
> coupled with his unsupported assertions that natural processes can be
> ruled out lead to the conclusion that he's arguing for a religious,
> not a scientific position
Well, of course, his touchy defensiveness about that question
indicates that, like the creation "scientists" and the ID "theorists",
he not only knows that he is arguing for his religious nopinions, but
also knows that he can't ADMIT that he is, and so must dishonestly
pretend that he's not.
It's just another reason why ID/creationists are deceptive evasive
dishonest liars. Every single one of them.
Fortunately for us, it's also why they will never win in court.
Ever. It is simply impossible to preach a religious opinion while at
the same time denying that one is preaching a religious opinion.
'Rev Dr' Lenny Flank
> On Dec 3, 12:06 am, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
>
>
> > It is of course entirely possible for two speices to have eaxtly the
> > same genes, nucleotide for nculeotide, and yet if one of them has a
> > large inverted section in a critical area, they won't be able to
> > produce viable offspring. So your entire assumption (interfertility
> > equals identity of "genetic information") is just a BS assumption on
> > yourn part that you can't demonstrate in any way whatsoever.
>
> > You've still not answered the most basic elementary of questions: How
> > do you measure this "distance in sequence space", and how can you
> > therefore show that humans and chimps are further apart in it than any
> > other two species are.
>
> for sean to tell you this will require that you provide him with
>
> -your mother's maiden name
> -your bank acct number
> -your SSN
> -your blood type
> -your 3rd girlfriend's great grandmother's middle name
>
> and any other irrelevant questions he can come up with
>
Oh, I am fully aware that Sean, like every other creationist I've met
over the past 25 years, will never answer a single direct question.
My questions make their point whether he answers them or not.
I didn't ask for, and I don't need, his cooperation.
When the sum total of Sean's argument is "chimps and humans differ too
widely by, uh, an unknown measurement", there's nothing for him to
answer questions ABOUT. He's simply not SAYING anything. (shrug)
'Rev Dr' Lenny Flank
> On Mon, 01 Dec 2008 19:55:29 -0800, Seanpit wrote:
> > [new DNA sequence appears]
> > Not necessarily. It just is unlikely to hit upon a new type of
> > function, a function that was not already in the genome pool to begin
> > with, that requires at least 600aa at minimum to work.
>
> How unlikely?
>
> To specific in my question: Suppose I give you a 600aa sequence, built by
> randomly selecting each site from available amino acids. What is the
> probability of it being functional? I am looking for the number and an
> explanation of how it was derived.
>
I'd like to see that too. Sean. If it's not, uh, another "unknown
measurement".
(snicker) (giggle)
'Rev Dr' Lenny Flank
> On Dec 2, 10:04 pm, Seanpit <sean...@gmail.com> wrote:
>
> Such differences are largely the
>
> > result of Mendelian-type variation within an otherwise static gene
> > pool of options.
>
> Would a descendent species that has a single chromosome produced by
> the fusion of two different chromosomes in its ancestor, count, in
> your view, as a "Mendelian-type variation within an otherwise static
> gene pool of options"?
>
> Even if it meant that the two species could no longer produce viable
> zygotes?
>
> Why nor why not?
>
A related question:
If the descendent species had a large inversion of gene sequence in a
critical area of its chromosome, as compared to its ancestor, which
prevented them from forming a viable zygote, would that too count, in
your view, as a "Mendelian-type variation within an otherwise static
gene pool of options"?
Why nor why not?
And perhaps you could expand upon your answer by citing an example of
the sort of hypothetical genetic change that you would consider to NOT
be a "Mendelian-type variation within an otherwise static gene pool of
options"?
And don't forget, I am still waiting to hear how we can measure "gaps
in sequence space", how we can tell whether the gap between species A
and B is larger than or smaller than the gap between species C and D,
and how you can calculate the, um, "statistical probability" of either
of these gaps being crossed when you, uh, don't know how big they are
or how to measure them. . . .
(And I'd prefer it greatly if you'd answer these simple questions,
rather than avoiding them and thereby making me ask them again and
again and again and again until you either answer or run away, like
most creationists do.)
Mark Isaak
>[snip]
> Fertility isn't an informational problem as much as it is a
> chromosomal structural problem.
Fertility is a fertility problem. A single mutation in a specific
compatibility gene can cause infertility; a million mutations and
chromosome rearrangements in other genes can leave things fertile.
'Rev Dr' Lenny Flank
I'm still waiting,
Sean . . . . . . . . . . . .. . . . . . . . . . . .
William Morse
> On 1 Dec, 23:21, Seanpit <seanpitnos...@naturalselection.0catch.com>
> wrote:
>> On 28 Nov, 10:24, geop...@hotmail.com wrote:
>>
>> > As I understand it, your whole problem with these amino acid systems
>> > is that, the larger they get, the fewer viable sequences there are of
>> > that size to mutate to.
>>
>> Size is only half of the problem. The other half is sequence
>> specificity. Just because a system has a large number of residues
>> doesn't mean that there is a significant degree of specificity for the
>> arrangement of the residues relative to each other. A large system with
>> low specificity can be on a much lower level of complexity than a much
>> smaller system with a higher degree of specificity.
>>
>> > I don't believe that size is the problem here, so I'd like to ask you
>> > a few questions about how these systems work.
>>
>> > 1) If I have a 300aa system, and that system is duplicated, is the
>> > result:
>>
>> > a) a 600aa system?
>>
>> Not necessarily. It is a 600aa sequence, but this sequence isn't
>> necessarily going to have a beneficial system of function attached to
>> it.
>
> I should add here that I'm basically equating 'gene sequences' to 'amino
> acid residues' (amino acid chains formed by concatenation of the amino
> acids output by translated DNA), but after a little research I see what
> you mean, and that the two don't quite mean the same
>
> My idea is that a sequence of DNA can be duplicated, which causes a
> structure to duplicate also, whether it's a whole protein or a piece of
> one. I believe what you're suggesting is that a duplication inside a
> protein would change its shape to something weird and make it
> unfunctional?
>
> If that's the case then I'm at the limit of my knowledge here, so I'll
> have to accept you may be correct. However, I've found that stuff is
> rarely black and white. It's a little like the whole evolution debate in
> microcosm, except instead of 'what use is half an eye?' it's now 'what
> use is half a protein'? Despite what Behe claims, I don't believe stuff
> is much more 'irreducible' at the molecular level.
>
>
>> > b) just 'two 300aa systems next to each other'?
>>
>> That can happen as well. Simple duplication doesn't make anything new.
>> It just makes more of the same thing. It is quantitative, not
>> qualitative, mutation.
>>
>> > c) something else?
>>
>> > If (a), then doesn't this prove that the size of a system is
>> > irrelevent to the ease of obtaining it?
>>
>> Simply producing a larger sequence with a multicharacter mutation isn't
>> enough to find a novel type of beneficial function that requires at
>> least that many fairly specified amino acid residues.
>>
>> For example, say that there is a specific 10-letter sequence that, if
>> found, would win you a million dollars. You know what the first 5
>> letters are. What are the odds that simply doubling your first five
>> letters, to make a 10-letter sequence, is going to end up being the
>> winning 10-letter sequence?
>>
>> See the point of the problem here?
>>
>>
> I can see yours, but I'm not sure I've made mine clear. It's not a
> question of probability if there's a multitude of goals.
>
>
>> > If (b), then I have further questions.
>>
>> > 2) If (b) was true, then this is just a couple of 300aa systems. Call
>> > them A and B. You claim that both of them have a larger number of
>> > viable systems they could mutate to, because they're smaller.
>>
>> That's right. The odds of finding a novel beneficial 300aa target are
>> exponentially greater than the odds of finding a novel 1000aa target
>> because the ratio of targets vs. non-targets is exponentially greater
>> at the 300aa level vs. the 1000aa level.
>>
>> > But now, suppose that a mutation in A makes it reliant on B. This
>> > could easily happen because B is providing the same functions as A,
>> > which allows A to give up some function and mutate it to something
>> > else.
>>
>> > Is the system now:
>>
>> > a) a 600aa system?
>>
>> Nope. It is still just a 300aa system that only became beneficial
>> because of a certain type of environment - an environment that includes
>> everything that already exists in a given genome.
>
> I don't get your meaning here.
>>
>> > b) still just two 300aa systems?
>>
>> Right . . .
>>
>> > c) something else?
>>
>> > If (a), then again, isn't it quite trivial to get these high aa
>> > systems?
>>
>> > If (b), then doesn't that mean that all high aa systems can be
>> > regarded as several low aa subsystems?
>>
>> No, because there are systems, like the flagellar system for example,
>> that require many thousands of fairly specified residues to be working
>> together at the same time in a specific orientation with each other for
>> the overall system to work. This is not the case with your two
>> separately acting 300aa systems. Because each residue in your two
>> systems does not have to be specifically arranged with all the other
>> 599 residues, this system is not very specified. It is therefore not
>> any more functionally complex than the most complex intact or specified
>> portion of the system - in this case 300 fsaars. This is why equally
>> large cascading systems made up of, say, 5 different proteins, are not
>> as functionally complex as a 5-protein system of equivalent numbers of
>> residues where all the individual protein parts must be specifically
>> arranged with each other in 3D space (and therefore all of the residues
>> as well).
>>
>> > 3) If (b) was true, then in theory, a 1000aa system can be a sum of
>> > many subsystems, and those subsystems may be considered low aa
>> > systems. In this case, doesn't this mean that a 1000aa system can
>> > easily find viable mutation possibilities, simply by mutations in its
>> > subsystems (which have many possibilities available)?
>>
>> You'd be correct if you were talking about a cascading system of
>> function where each part was not required to be specifically arranged
>> in 3D space with all the other parts at the same time.
>
> Well, I believe that most arrangements are more like this and not quite
> as specific as you believe, seeing as the argument from specificity
> often fails when applied to other stuff when it fails to consider every
> option. However, I'd have to ask a molecular biologist about that.
>
> Thanks for answering the questions.
I think you should thank Sean for responding, rather than for answering
the questions. Because his answers were largely obfuscation in response
to legitimate questions on your part. First off, even in large proteins
with many amino acids, most of them are not all that important to the
protein function. Even in hemoglobin, where the functional sequence is
highly conserved, we are talking about tens of amino acids at the binding
site. Many of the rest can change between a number of amino acids that
behave similarly in protein folding without significantly affecting the
function.
Hemoglobin is also instructive because it is composed of several
subunits, which have in fact combined to produce a system of greater
complexity. So you are on the right track. You seem to have a decent
intuition of how this stuff works, and I would encourage you to read the
science. Think of Sean Pitman as a devil's advocate - when you understand
the science you will know why he is wrong.
Yours,
Bill Morse
seanpi...@naturalselection.0catch.com
Not true. You don't seem to understand the difference between meiosis
and mitosis.
For example, if a piece of donkey chromosome is inverted relative to
its counterpart in horses, then gene-by-gene pairing cannot occur
without elaborate looping and twisting. The chance of a successful
cell division is very much reduced. So, the mule cannot make egg or
sperm cells. Thus, the mule is sterile. However, a mule can still be
born healthy because such growth of non-meiotic cells occurs via a
different process called mitosis. Mitosis does not have to match
things up; it only has to make copies. So, inversions and
translocations do not prevent the mule from growing up to be an adult.
Perhaps a little refresher course in genetics is in order?
http://www.detectingdesign.com/donkeyshorsesmules.html
> So your entire assumption (interfertility
> equals identity of "genetic information") is just a BS assumption on
> yourn part that you can't demonstrate in any way whatsoever.
You just don't understand the genetics involved.
> You've still not answered the most basic elementary of questions: How
> do you measure this "distance in sequence space", and how can you
> therefore show that humans and chimps are further apart in it than any
> other two species are.
I've already told you several times. You can know that they are
likely further, but by how much is not knowable yet. You know that
they are further because they cannot produce viable much less fertile
offspring. Try to remember this time.
< snip rest >
Sean Pitman
www.DetectingDesign.com
seanpi...@naturalselection.0catch.com
Not true. You don't seem to understand the difference between meiosis
and mitosis.
For example, if a piece of donkey chromosome is inverted relative to
its counterpart in horses, then gene-by-gene pairing cannot occur
without elaborate looping and twisting. The chance of a successful
cell division is very much reduced. So, the mule cannot make egg or
sperm cells. Thus, the mule is sterile. However, a mule can still be
born healthy because such growth of non-meiotic cells occurs via a
different process called mitosis. Mitosis does not have to match
things up; it only has to make copies. So, inversions and
translocations do not prevent the mule from growing up to be an adult.
Perhaps a little refresher course in genetics is in order?
http://www.detectingdesign.com/donkeyshorsesmules.html
> So your entire assumption (interfertility
> equals identity of "genetic information") is just a BS assumption on
> yourn part that you can't demonstrate in any way whatsoever.
You just don't understand the genetics involved.
> You've still not answered the most basic elementary of questions: How
> do you measure this "distance in sequence space", and how can you
> therefore show that humans and chimps are further apart in it than any
> other two species are.
I've already told you several times. You can know that they are
seanpi...@naturalselection.0catch.com
Not true. You don't seem to understand the difference between meiosis
and mitosis.
For example, if a piece of donkey chromosome is inverted relative to
its counterpart in horses, then gene-by-gene pairing cannot occur
without elaborate looping and twisting. The chance of a successful
cell division is very much reduced. So, the mule cannot make egg or
sperm cells. Thus, the mule is sterile. However, a mule can still be
born healthy because such growth of non-meiotic cells occurs via a
different process called mitosis. Mitosis does not have to match
things up; it only has to make copies. So, inversions and
translocations do not prevent the mule from growing up to be an adult.
Perhaps a little refresher course in genetics is in order?
http://www.detectingdesign.com/donkeyshorsesmules.html
> So your entire assumption (interfertility
> equals identity of "genetic information") is just a BS assumption on
> yourn part that you can't demonstrate in any way whatsoever.
You just don't understand the genetics involved.
> You've still not answered the most basic elementary of questions: How
> do you measure this "distance in sequence space", and how can you
> therefore show that humans and chimps are further apart in it than any
> other two species are.
I've already told you several times. You can know that they are
seanpi...@naturalselection.0catch.com
seanpi...@naturalselection.0catch.com
Not true. You don't seem to understand the difference between meiosis
and mitosis.
For example, if a piece of donkey chromosome is inverted relative to
its counterpart in horses, then gene-by-gene pairing cannot occur
without elaborate looping and twisting. The chance of a successful
cell division is very much reduced. So, the mule cannot make egg or
sperm cells. Thus, the mule is sterile. However, a mule can still be
born healthy because such growth of non-meiotic cells occurs via a
different process called mitosis. Mitosis does not have to match
things up; it only has to make copies. So, inversions and
translocations do not prevent the mule from growing up to be an adult.
Perhaps a little refresher course in genetics is in order?
http://www.detectingdesign.com/donkeyshorsesmules.html
> So your entire assumption (interfertility
> equals identity of "genetic information") is just a BS assumption on
> yourn part that you can't demonstrate in any way whatsoever.
You just don't understand the genetics involved.
> You've still not answered the most basic elementary of questions: How
> do you measure this "distance in sequence space", and how can you
> therefore show that humans and chimps are further apart in it than any
> other two species are.
I've already told you several times. You can know that they are
seanpi...@naturalselection.0catch.com
Not true. You don't seem to understand the difference between meiosis
and mitosis.
For example, if a piece of donkey chromosome is inverted relative to
its counterpart in horses, then gene-by-gene pairing cannot occur
without elaborate looping and twisting. The chance of a successful
cell division is very much reduced. So, the mule cannot make egg or
sperm cells. Thus, the mule is sterile. However, a mule can still be
born healthy because such growth of non-meiotic cells occurs via a
different process called mitosis. Mitosis does not have to match
things up; it only has to make copies. So, inversions and
translocations do not prevent the mule from growing up to be an adult.
Perhaps a little refresher course in genetics is in order?
http://www.detectingdesign.com/donkeyshorsesmules.html
> So your entire assumption (interfertility
> equals identity of "genetic information") is just a BS assumption on
> yourn part that you can't demonstrate in any way whatsoever.
You just don't understand the genetics involved.
> You've still not answered the most basic elementary of questions: How
> do you measure this "distance in sequence space", and how can you
> therefore show that humans and chimps are further apart in it than any
> other two species are.
I've already told you several times. You can know that they are
seanpi...@naturalselection.0catch.com
Not true. You don't seem to understand the difference between meiosis
and mitosis.
For example, if a piece of donkey chromosome is inverted relative to
its counterpart in horses, then gene-by-gene pairing cannot occur
without elaborate looping and twisting. The chance of a successful
cell division is very much reduced. So, the mule cannot make egg or
sperm cells. Thus, the mule is sterile. However, a mule can still be
born healthy because such growth of non-meiotic cells occurs via a
different process called mitosis. Mitosis does not have to match
things up; it only has to make copies. So, inversions and
translocations do not prevent the mule from growing up to be an adult.
Perhaps a little refresher course in genetics is in order?
http://www.detectingdesign.com/donkeyshorsesmules.html
> So your entire assumption (interfertility
> equals identity of "genetic information") is just a BS assumption on
> yourn part that you can't demonstrate in any way whatsoever.
You just don't understand the genetics involved.
> You've still not answered the most basic elementary of questions: How
> do you measure this "distance in sequence space", and how can you
> therefore show that humans and chimps are further apart in it than any
> other two species are.
I've already told you several times. You can know that they are
'Rev Dr' Lenny Flank
> For example, if a piece of donkey chromosome is inverted relative to
> its counterpart in horses, then gene-by-gene pairing cannot occur
> without elaborate looping and twisting. The chance of a successful
> cell division is very much reduced. So, the mule cannot make egg or
> sperm cells. Thus, the mule is sterile.
And what happens, Sean, when a descendent species which has a piece of
its chromosome inverted rleative to its ancestor, tries to interbreed
with that ancestor . . . . . . .?
However, a mule can still be
> born healthy because such growth of non-meiotic cells occurs via a
> different process called mitosis. Mitosis does not have to match
> things up; it only has to make copies. So, inversions and
> translocations do not prevent the mule from growing up to be an adult.
>
> Perhaps a little refresher course in genetics is in order?
Perhaps a little reading comprehension is in order, since this wasn't
what I was asking about.
> You just don't understand the genetics involved.
Then educate me, Sean. Share your superior knowledge and
understanding with me.
> > You've still not answered the most basic elementary of questions: How
> > do you measure this "distance in sequence space", and how can you
> > therefore show that humans and chimps are further apart in it than any
> > other two species are.
>
> I've already told you several times. You can know that they are
> likely further, but by how much is not knowable yet. You know that
> they are further because they cannot produce viable much less fertile
> offspring. Try to remember this time.
I remember just fine. You can't measure it, you can't even define it,
but you "know" that it's larger in humans/chimps than other species.
Yeah, Sean, I think I understand you perfectly.
'Rev Dr' Lenny Flank
What's a "information problem"?
seanpi...@naturalselection.0catch.com
wrote:
> Seanpit wrote:
> > On 2 Dec, 15:58, John Harshman <jharshman.diespam...@pacbell.net>
> > wrote:
> >>>> Um, humans and chimps are 98.5% identical in their DNA.
> >>> Depends on what part of the genome you're looking at. This 98.5%
> >>> number is usually based on homologies of protein-coding genes.
> >> Wrong. It's based on the overall percent identity of all sequences with
> >> homologs present in both species. Since protein-coding (and other
> >> conserved) sequences are a tiny minority of the genome, in effect it's
> >> an assay of junk DNA. Protein-coding sequences are on average 99.5%
> >> identical between species.
>
> > Most estimates of sequence divergence have focused exclusively on base
> > substitutions in DNA—that is, one base (or one DNA ‘letter’—A, T, C or
> > G) being replaced with another. More recent calculations also include
> > insertions and deletions, or indels, in addition to base
> > substitutions.
>
> No, those aren't more recent calculations. They're just different. None
> of the numbers you have quoted have anything to do with counting indels.
> What follows here is more of your "baffling with bullshit" tactic. When
> you're wrong, you just cite irrelevant studies.
They're published in mainstream literature. I guess you get to decide
what is and is not relevant in science?
> > The author of one such study, Roy J. Britten, argues:
>
> > "It appears appropriate to me to consider the full length of the
> > gaps in estimating the interspecies divergence. These stretches of DNA
> > are actually absent from one and present in the other genome. In the
> > past, indels have often simply been counted regardless of length and
> > added to the base substitution count, because that is convenient for
> > phylogenetics."
>
> Yes, and I think Britten's idea is silly. What biological reason is
> there to count the lengths of gaps, when each gap is generally a single
> mutation? A 1-base gap is 1 mutation; a thousand-base gap is 1 mutation.
A difference of 1000 bp could be functionally significant - regardless
of how it was produced. That is why Britten's method makes much more
sense than only counting non-gap regions of DNA.
> > Britten, R.J., Divergence between samples of chimpanzee and human DNA
> > sequences is 5%, counting indels, Proc. Nat. Acad. Sci. USA 99(21):
> > 13633–13635, 2002.
>
> > His findings lend support to the idea that much of the failure of DNA
> > to hybridize between chimps and humans is the result of missing DNA
> > due to indel events.
>
> What failure to hybridize are you talking about here? Perhaps you mean
> that most sequences that don't hybridize are those that are not shared.
> That makes sense, as the other reason for having a non-hybridized
> fraction in a DNA-DNA hybridization experiment is high sequence
> divergence, which isn't going to happen between humans and chimps.
Exactly . . .
> > Britten then became involved in a follow-up paper in which these
> > initial results were confirmed; in fact, it was found that "the 5%
> > human-chimp difference already published is likely to be an
> > underestimate, possibly by more than a factor of 2." - - in other
> > words by more than 10%.
>
> Again, the estimate is biologically meaningless.
How do you know? . . .
> > Britten, R.J., Rowen, L., Williams, J. and Cameron, R.A., Majority of
> > divergence between closely related DNA samples is due to indels, Proc.
> > Nat. Acad. Sci. USA 100(8):4661–4665, 2003.
>
> > Then, Anzai et al. published a study where nearly one-half of the MHC
> > region was sequenced - within chimps. The sequence results in
> > comparison the the human region actually dropped the DNA similarity
> > estimate down to 86.7%. Anzai concluded that the 86.7% estimate "may
> > be a better representation of whole-genome sequence similarity between
> > the human and the chimpanzee" than previous estimates of 98.6% since
> > "the major difference between the human and chimpanzee sequences is
> > overwhelmingly attributable to indels".
>
> Once again, biologically meaningless.
Based only on your say so . . .
> > Anzai, T., Shiina, T., Kimura, N., Yanagiya, K., Kohara, S.,
> > Shigenari, A., Yamagata, T., Kulski, J.K., Naruse, T.K., Fujimori, Y.,
> > Fukuzumi, Y., Yamazaki, M., Tashiro, H., Iawmoto, C., Umehara, Y.,
> > Imanishi, T., Meyer, A., Ikeo, K., Gojobori, T., Bahram, S. and Inoko,
> > H., Comparative sequencing of human and chimpanzee MHC class I regions
> > unveils insertions/deletions as the major path to genomic divergence,
> > Proc. Nat. Acad. Sci. USA 100(13):7708–7713, 2003.
>
> > Of course, other studies, have resulted in estimates of similarity
> > higher than 98.6%. For instance, Wildman et al.compared ~90 kilobases
> > of human DNA to chimps and found a similarity of 98.86%, even when
> > counting indels.
>
> > Wildman, D.E., Uddin, M., Liu, G., Grossman, L.I. and Goodman, M.,
> > Implications of natural selection in shaping 99.4% nonsynonymous DNA
> > identity between humans and chimpanzees: enlarging genus Homo, Proc.
> > Nat. Acad. Sci. USA 100(12):7181–7188, 2003.
>
> > This seems to be in direct opposition to the data presented by Britten
> > and Anzai et al. However, Wildman’s team examined only coding DNA from
> > a number of genes. Britten and Anzai both considered non-coding DNA in
> > their studies and therefore consider a greater range of DNA types in
> > their conclusion of an 86.7 similarity.
>
> Blah, blah. More irrelevant nonsense, except that you provide a quote
> for my statement that protein-coding regions average 99.5% identity.
Just bricks and mortar - not the main informational source within DNA.
> > See also:
> >http://www.answersingenesis.org/tj/v18/i2/similarity.asp
>
> >>> However, non-coding functional DNA elements, like miRNA producing
> >>> regions of the genome, can be much more different. For example,
> >>> miRNAs from the brains of humans and chimps show an overlap of only
> >>> 83%.
> >> What exactly does this mean? Are you talking about the genome or about
> >> expression patterns?
>
> > Both . . .
>
> Not good. You need to untangle them if you want to know what's happening.
Not needed in this case . . .
> >>> "miRNAs recently have been implicated in synaptic development and
> >>> in memory formation. As the species specific miRNAs described here are
> >>> expressed in the brain, which is the most complex tissue in the human
> >>> body, with an estimated 10,000 different cell types, these miRNAs
> >>> could have a role in establishing or maintaining cellular diversity
> >>> and could thereby contribute to the differences in human and
> >>> chimpanzee brain ... function."
> >>>http://www.niob.knaw.nl/researchpages/cuppen/publications/berezikov_N...
> >> Ah, it is indeed expression pattern, though they did search the genomes
> >> for recovered sequences. So 83% of candidate miRNAs recovered in this
> >> particular expression study were found in both genomes. Note that many
> >> of these miRNAs are parts of families that have been duplicated, with
> >> divergence, either in human or chimp, so there is a known mechanism
> >> responsible for at least some of the difference. I note also that the
> >> percentage of miRNAs in common between species pairs follows exactly the
> >> pattern expected from phylogeny.
>
> > All bets are off when NS is involved as a preserving force over
> > time. Here we have 17% miRNAs that are not homologous between species
> > - and that is just one type of non-coding potentially functional DNA
> > type. This isn't just an expression pattern. This represents unique
> > genomic differences that are likely functionally important.
>
> Again, it's 17% of the candidate miRNAs that were recovered in a
> particular expression study that are not *orthologous* to one in the
> other species.
And what reason is there to think that this sampling is not
representative of all miRNAs? - and the underlying DNA sequences upon
which they are based?
> >>>> That is closer than most of the other species which creationists
> >>>> assume "microevolved".
> >>> It isn't as clear cut as you make it out to be. The functional
> >>> differences between humans and apes are not clearly understood on a
> >>> genetic level yet.
> >> Well enough that it seems unlikely there could be any huge neutral gaps
> >> hiding in the genetic differences.
>
> > You can't say that unless you actually know something about the end-
> > product functional differences - differences that may be and are
> > likely the result of many miRNAs and other non-coding elements using
> > similar gene-product building blocks to build functionally novel
> > systems. This is in fact suggested to be the reason for structural
> > and functional differences between the brains of humans and chimps.
>
> And it may be part of the reason. But miRNAs are short and can easily
> evolve. We also have no data suggesting that any of this requires
> crossing of any large, neutral gap, and every reason to believe that
> individual mutations could be selectively advantageous.
It isn't the miRNA's one at a time that is important here. It is the
end-product system that is important here. If the end-product system
requires multiple miRNAs to produce its unique structural features, at
minimum, the problem isn't going to be solved by explaining how to get
one miRNA at a time since a minimum of many are required before the
minimum structural requirements of the system in question can be
realized.
> >> [snip Sean's "baffle with bullshit" phase]
>
> > What? You think the fact that humans and apes do not produce viable
> > much less fertile offspring is irrelevant?
>
> Yes. Some closely related species can't produce viable offspring. Some
> distantly related species can. There is no particular correlation
> between closeness of relationship and hybridization.
Ah, care to provide some actual examples?
I say that there is a very good correlation between qualitative
functional aspects of a gene pool and hybridization. Allelic
variations with the same qualitative function aren't in question
here. Many quantitative differences can exist between gene pools -
just as long as the qualitative functional features and options are
the same.
> > How is the presentation of
> > examples of interbreeding species that produce at least viable and
> > even occasionally fertile offspring at all germane when it comes to
> > the argument that humans and chimps are even more closely related?
>
> It isn't. Nor is the inability of chimps and humans to hybridize.
Think again. One of the very foundations of the concept of
"speciation" involves the ability to successful mate and interbreed.
This means producing both viable and fertile offspring. If at least
the viability part of this equation is intact in one pairing, but not
another, which pairing most likely represents a more functionally
"close" or "similar" pairing?
> > even though they cannot produce viable much less fertile offspring?
> > Who's BSing here?
>
> You are, as I've already mentioned several times.
LOL - right ; )
Sean Pitman
www.DetectingDesign.com
'Rev Dr' Lenny Flank
>
> Based only on your say so . . .
Speaking of which . . .
Can you explain to me one more time, Sean, (1) how you measure the
"gap" in "sequence space" and (2) what measurements you can use to
demonstrate that the human/chimp "gap" is larger than the gap between,
say, jaguars and cheetahs, or boas and pythons, or any other two
species?
Other than "I just know so" . . . ?
'Rev Dr' Lenny Flank
And still waiting . . . . . . . . .
hersheyh
I do. You, however, have a simplistic view of what happens when there
are chromosomal rearrangements like inversions.
>
> For example, if a piece of donkey chromosome is inverted relative to
> its counterpart in horses, then gene-by-gene pairing cannot occur
> without elaborate looping and twisting. The chance of a successful
> cell division is very much reduced.
It is true that *when* there is a crossover within an inverted region,
for the two (out of four) chromatids involved in the crossover that
you do get duplication or deletion of information and, depnding on the
location, acentric and dicentric chromatids.
No chromosomal aberration in meiosis occurs if there is no crossover
within the inverted region.
So for those meioses in which crossovers occur within an inversion,
half of the time, *in theory*, you might get an inviable gamete. *In
practice* it depends on the species. In corn, for example, dicentric
chromosomes break, leading to the possibility of an egg getting an
aberrant chromosome (and half of pollen getting aberrations). In
Drosophila, OTOH, dicentric chromatids do not break and typically wind
up in the polar bodies rather than the egg. And produce ineffective
double-headed sperm. So the aberrations do not reach the stage of
being in the gametes, whereas the chromatids not involved in crossing
over do get into functional sperm and egg.
Meioses in which there has been no intra-inversion crossing over
produce perfectly normal eggs and sperm in perfectly normal amounts.
The reduction in fertility, then, is a lot less than one might expect
*unless* there are multiple or very large inversions. Significant
reduction in fertility often requires multiple chromosome
rearrangement, not just one.
BTW, there are multiple rearrangement differences between humans and
chimp, but as the mule (and the more pathetic hinny) shows, that does
not prevent viability of the hybrid. For the reason why humans and
chimps do not produce viable hybrids, you have to look elsewhere.
> So, the mule cannot make egg or
> sperm cells. Thus, the mule is sterile. However, a mule can still be
> born healthy because such growth of non-meiotic cells occurs via a
> different process called mitosis. Mitosis does not have to match
> things up; it only has to make copies. So, inversions and
> translocations do not prevent the mule from growing up to be an adult.
>
> Perhaps a little refresher course in genetics is in order?
Yes. You do need to take one.
>
> http://www.detectingdesign.com/donkeyshorsesmules.html
>
> > So your entire assumption (interfertility
> > equals identity of "genetic information") is just a BS assumption on
> > yourn part that you can't demonstrate in any way whatsoever.
>
> You just don't understand the genetics involved.
>
> > You've still not answered the most basic elementary of questions: How
> > do you measure this "distance in sequence space", and how can you
> > therefore show that humans and chimps are further apart in it than any
> > other two species are.
>
> I've already told you several times. You can know that they are
> likely further, but by how much is not knowable yet.
What we know is that there is no sequence difference in any gene or
even any length of DNA sequence between chimps and humans that is
unaccountable for by the known rates of change that can be permitted
by selection for change. In fact, there are almost no genes or
lengths of DNA with more change than would be expected by neutral
drift from a common ancestor in the time available. There is nothing
in the amount of change in DNA sequences between human and chimp that
requires non-natural or exceptionally rapid intervention by an outside
agent, intelligent or otherwise.
> You know that
> they are further because they cannot produce viable much less fertile
> offspring. Try to remember this time.
In the case of human and chimp, the reason for inviability of hybrids
would most likely lie in differences in rates of development of
various organs leading to early lethality due to developmental
discord. It would not be due to chromosomal rearrangements.
>
> < snip rest >
>
> Sean Pitmanwww.DetectingDesign.com
Steven L.
> On 28 Nov, 10:24, geop...@hotmail.com wrote:
>> As I understand it, your whole problem with these amino acid systems
>> is that, the larger they get, the fewer viable sequences there are of
>> that size to mutate to.
>
> Size is only half of the problem. The other half is sequence
> specificity. Just because a system has a large number of residues
> doesn't mean that there is a significant degree of specificity for the
> arrangement of the residues relative to each other. A large system
> with low specificity can be on a much lower level of complexity than a
> much smaller system with a higher degree of specificity.
>
>> I don't believe that size is the problem here, so I'd like to ask you
>> a few questions about how these systems work.
>>
>> 1) If I have a 300aa system, and that system is duplicated, is the
>> result:
>>
>> a) a 600aa system?
>
> Not necessarily. It is a 600aa sequence, but this sequence isn't
> necessarily going to have a beneficial system of function attached to
> it.
>
>
> That can happen as well. Simple duplication doesn't make anything
> new. It just makes more of the same thing. It is quantitative, not
> qualitative, mutation.
>
>> c) something else?
>>
>> If (a), then doesn't this prove that the size of a system is
>> irrelevent to the ease of obtaining it?
>
> Simply producing a larger sequence with a multicharacter mutation
> isn't enough to find a novel type of beneficial function that requires
> at least that many fairly specified amino acid residues.
>
> For example, say that there is a specific 10-letter sequence that, if
> found, would win you a million dollars. You know what the first 5
> letters are. What are the odds that simply doubling your first five
> letters, to make a 10-letter sequence, is going to end up being the
> winning 10-letter sequence?
The odds against winning a state lottery are comparably high. But in
most lottery draws, at least one player does win. I may not win, and
you may not win, but *somebody* *somewhere* is going to win.
You keep focusing on how difficult it would be for a *single* amino acid
residue to evolve new beneficial function. But how about considering a
quintillion amino acid residues, all capable of mutation, all contained
within respective organisms that will reproduce and leave those
mutations to progeny? Can *at least* one out of a quintillion organisms
produce such a favorable mutation?
Have you even considered how many single-celled organisms might have
been living in the oceans of the pre-Cambrian era? I keep telling you,
you need to consider the mathematical expectation: The (admittedly
small) probability of a favorable amino acid change, multiplied by the
astronomically high number of organisms that had existed. Or if you
want to go back to abiogenesis, the astronomically high number of
organic molecules that had existed.
Today, it is estimated that there are some 10^30 bacteria on earth.
That is such an astronomically high number that *any* favorable
bacterial mutation you can imagine, even if the odds against it
occurring are a trillion to one, is a virtual certainty to occur
somewhere on earth today. Whether that organism survives long enough to
reproduce progeny is, of course, also a matter of luck.
--
Steven L.
Email: sdli...@earthlinkNOSPAM.net
Remove the NOSPAM before replying to me.
John Harshman
We all do. I have stated my reasons. What's wrong with them?
>>> The author of one such study, Roy J. Britten, argues:
>>> "It appears appropriate to me to consider the full length of the
>>> gaps in estimating the interspecies divergence. These stretches of DNA
>>> are actually absent from one and present in the other genome. In the
>>> past, indels have often simply been counted regardless of length and
>>> added to the base substitution count, because that is convenient for
>>> phylogenetics."
>> Yes, and I think Britten's idea is silly. What biological reason is
>> there to count the lengths of gaps, when each gap is generally a single
>> mutation? A 1-base gap is 1 mutation; a thousand-base gap is 1 mutation.
>
> A difference of 1000 bp could be functionally significant - regardless
> of how it was produced. That is why Britten's method makes much more
> sense than only counting non-gap regions of DNA.
What makes the most sense is counting mutations. Humans and chimps
differ by 40 million mutations. 35 million of those are point
substitutions. 5 million are indels. There are a negligible few more
that don't fall into either category, such as chromosomal fusions,
inversions, and perhaps a few more categories I'm not thinking of.
A difference of 1000bp could be functionally significant, and so could a
single point substitution. So? I'm not saying you should count only
non-gap regions. I'm saying you should count one mutation as one
mutation. A 10-base indel is not any more or less a single mutation than
a 1000-base indel.
>>> Britten, R.J., Divergence between samples of chimpanzee and human DNA
>>> sequences is 5%, counting indels, Proc. Nat. Acad. Sci. USA 99(21):
>>> 13633–13635, 2002.
>>> His findings lend support to the idea that much of the failure of DNA
>>> to hybridize between chimps and humans is the result of missing DNA
>>> due to indel events.
>> What failure to hybridize are you talking about here? Perhaps you mean
>> that most sequences that don't hybridize are those that are not shared.
>> That makes sense, as the other reason for having a non-hybridized
>> fraction in a DNA-DNA hybridization experiment is high sequence
>> divergence, which isn't going to happen between humans and chimps.
>
> Exactly . . .
So?
>>> Britten then became involved in a follow-up paper in which these
>>> initial results were confirmed; in fact, it was found that "the 5%
>>> human-chimp difference already published is likely to be an
>>> underestimate, possibly by more than a factor of 2." - - in other
>>> words by more than 10%.
>> Again, the estimate is biologically meaningless.
>
> How do you know? . . .
Explain its biological meaning.
>>> Britten, R.J., Rowen, L., Williams, J. and Cameron, R.A., Majority of
>>> divergence between closely related DNA samples is due to indels, Proc.
>>> Nat. Acad. Sci. USA 100(8):4661–4665, 2003.
>>> Then, Anzai et al. published a study where nearly one-half of the MHC
>>> region was sequenced - within chimps. The sequence results in
>>> comparison the the human region actually dropped the DNA similarity
>>> estimate down to 86.7%. Anzai concluded that the 86.7% estimate "may
>>> be a better representation of whole-genome sequence similarity between
>>> the human and the chimpanzee" than previous estimates of 98.6% since
>>> "the major difference between the human and chimpanzee sequences is
>>> overwhelmingly attributable to indels".
>> Once again, biologically meaningless.
>
> Based only on your say so . . .
I have given my reasons. Feel free to argue with them.
>>> Anzai, T., Shiina, T., Kimura, N., Yanagiya, K., Kohara, S.,
>>> Shigenari, A., Yamagata, T., Kulski, J.K., Naruse, T.K., Fujimori, Y.,
>>> Fukuzumi, Y., Yamazaki, M., Tashiro, H., Iawmoto, C., Umehara, Y.,
>>> Imanishi, T., Meyer, A., Ikeo, K., Gojobori, T., Bahram, S. and Inoko,
>>> H., Comparative sequencing of human and chimpanzee MHC class I regions
>>> unveils insertions/deletions as the major path to genomic divergence,
>>> Proc. Nat. Acad. Sci. USA 100(13):7708–7713, 2003.
>>> Of course, other studies, have resulted in estimates of similarity
>>> higher than 98.6%. For instance, Wildman et al.compared ~90 kilobases
>>> of human DNA to chimps and found a similarity of 98.86%, even when
>>> counting indels.
>>> Wildman, D.E., Uddin, M., Liu, G., Grossman, L.I. and Goodman, M.,
>>> Implications of natural selection in shaping 99.4% nonsynonymous DNA
>>> identity between humans and chimpanzees: enlarging genus Homo, Proc.
>>> Nat. Acad. Sci. USA 100(12):7181–7188, 2003.
>>> This seems to be in direct opposition to the data presented by Britten
>>> and Anzai et al. However, Wildman’s team examined only coding DNA from
>>> a number of genes. Britten and Anzai both considered non-coding DNA in
>>> their studies and therefore consider a greater range of DNA types in
>>> their conclusion of an 86.7 similarity.
>> Blah, blah. More irrelevant nonsense, except that you provide a quote
>> for my statement that protein-coding regions average 99.5% identity.
>
> Just bricks and mortar - not the main informational source within DNA.
I agree that most of the significant differences between humans and
chimps are probably in non-coding DNA, if that's what you mean. I don't
know your definition of information, so can't be sure what you meant to
say. I just point out that your initial assertion about the nature of
that 98.5% similarity is wrong, based on what you yourself have quoted.
>>> See also:
>>> http://www.answersingenesis.org/tj/v18/i2/similarity.asp
>>>>> However, non-coding functional DNA elements, like miRNA producing
>>>>> regions of the genome, can be much more different. For example,
>>>>> miRNAs from the brains of humans and chimps show an overlap of only
>>>>> 83%.
>>>> What exactly does this mean? Are you talking about the genome or about
>>>> expression patterns?
>>> Both . . .
>> Not good. You need to untangle them if you want to know what's happening.
>
> Not needed in this case . . .
Why?
What reason is there to think it is? I suspect the brain tissue was
chosen for this study based on the assumption that it's not
representative, but is a tissue of special importance in human evolution.
>>>>>> That is closer than most of the other species which creationists
>>>>>> assume "microevolved".
>>>>> It isn't as clear cut as you make it out to be. The functional
>>>>> differences between humans and apes are not clearly understood on a
>>>>> genetic level yet.
>>>> Well enough that it seems unlikely there could be any huge neutral gaps
>>>> hiding in the genetic differences.
>>> You can't say that unless you actually know something about the end-
>>> product functional differences - differences that may be and are
>>> likely the result of many miRNAs and other non-coding elements using
>>> similar gene-product building blocks to build functionally novel
>>> systems. This is in fact suggested to be the reason for structural
>>> and functional differences between the brains of humans and chimps.
>> And it may be part of the reason. But miRNAs are short and can easily
>> evolve. We also have no data suggesting that any of this requires
>> crossing of any large, neutral gap, and every reason to believe that
>> individual mutations could be selectively advantageous.
>
> It isn't the miRNA's one at a time that is important here. It is the
> end-product system that is important here. If the end-product system
> requires multiple miRNAs to produce its unique structural features, at
> minimum, the problem isn't going to be solved by explaining how to get
> one miRNA at a time since a minimum of many are required before the
> minimum structural requirements of the system in question can be
> realized.
We have no reason to believe that multiple miRNAs must have been
inserted simultaneously, or that they couldn't have evolved one at a
time. You have no evidence for your claim that a "minimum of many" is
necessary. And in fact if this is about brain size, the fossil record
shows a gradual increase over millions of years.
>>>> [snip Sean's "baffle with bullshit" phase]
>>> What? You think the fact that humans and apes do not produce viable
>>> much less fertile offspring is irrelevant?
>> Yes. Some closely related species can't produce viable offspring. Some
>> distantly related species can. There is no particular correlation
>> between closeness of relationship and hybridization.
>
> Ah, care to provide some actual examples?
The problem with this is that I don't know what you are willing to
consider related, since I have no idea what a "kind" is supposed to be.
But this is a commonplace fact of science.
> I say that there is a very good correlation between qualitative
> functional aspects of a gene pool and hybridization. Allelic
> variations with the same qualitative function aren't in question
> here. Many quantitative differences can exist between gene pools -
> just as long as the qualitative functional features and options are
> the same.
That's fine for you, because the undefined nature of "qualitative
functional features and options", being known only to you, makes it
possible for you to ignore any examples I might bring out.
But let's try. Does the entire family Anatidae share all the same
qualitative functions?
>>> How is the presentation of
>>> examples of interbreeding species that produce at least viable and
>>> even occasionally fertile offspring at all germane when it comes to
>>> the argument that humans and chimps are even more closely related?
>> It isn't. Nor is the inability of chimps and humans to hybridize.
>
> Think again. One of the very foundations of the concept of
> "speciation" involves the ability to successful mate and interbreed.
That was a bizarre non sequitur, and I have no idea how to respond.
> This means producing both viable and fertile offspring. If at least
> the viability part of this equation is intact in one pairing, but not
> another, which pairing most likely represents a more functionally
> "close" or "similar" pairing?
I have no idea, since none of your terms are defined. How do we
determine functional similarity?
>>> even though they cannot produce viable much less fertile offspring?
>>> Who's BSing here?
>> You are, as I've already mentioned several times.
>
> LOL - right ; )
Thanks for admitting that, at least.
John Harshman
> On Dec 3, 10:52 pm, seanpitnos...@naturalselection.0catch.com wrote:
[snip]
>>> You've still not answered the most basic elementary of questions: How
>>> do you measure this "distance in sequence space", and how can you
>>> therefore show that humans and chimps are further apart in it than any
>>> other two species are.
>> I've already told you several times. You can know that they are
>> likely further, but by how much is not knowable yet. You know that
>> they are further because they cannot produce viable much less fertile
>> offspring. Try to remember this time.
>
>
> I remember just fine. You can't measure it, you can't even define it,
> but you "know" that it's larger in humans/chimps than other species.
>
> Yeah, Sean, I think I understand you perfectly.
I don't believe you do, quite. Sean appears to be saying that genetic
distance is equivalent to ability to interbreed. If two species can't
interbreed, they are by definition more genetically distant than two
species that can. I don't think he's making a claim about sequence
similarity at all. He's merely advancing his own personal measure of
genetic distance. And of course his own personal measure is highly
correlated with his own personal measure. By definition.
seanpi...@naturalselection.0catch.com
>
> > > It is of course entirely possible for two speices to have eaxtly the
> > > same genes, nucleotide for nculeotide, and yet if one of them has a
> > > large inverted section in a critical area, they won't be able to
> > > produce viable offspring.
>
> > Not true. You don't seem to understand the difference between meiosis
> > and mitosis.
>
> I do. You, however, have a simplistic view of what happens when there
> are chromosomal rearrangements like inversions.
Really . . .
> > For example, if a piece of donkey chromosome is inverted relative to
> > its counterpart in horses, then gene-by-gene pairing cannot occur
> > without elaborate looping and twisting. The chance of a successful
> > cell division is very much reduced.
>
> It is true that *when* there is a crossover within an inverted region,
> for the two (out of four) chromatids involved in the crossover that
> you do get duplication or deletion of information and, depnding on the
> location, acentric and dicentric chromatids.
> No chromosomal aberration in meiosis occurs if there is no crossover
> within the inverted region.
That's right. It is only when the inverted region is likely to
sustain a crossover event that there is usually a problem. This is in
fact commonly a problem for mules. That is why, although there are
rare reported cases of mule fertility, that mules are considered
sterile.
> So for those meioses in which crossovers occur within an inversion,
> half of the time, *in theory*, you might get an inviable gamete.
More than have the time, far more, depending on the likelihood of a
crossover event within the inverted region.
> *In
> practice* it depends on the species. In corn, for example, dicentric
> chromosomes break, leading to the possibility of an egg getting an
> aberrant chromosome (and half of pollen getting aberrations).
Dicentric chromosomes aren't the same thing as chromosomal
inversions. If one chromosome is dicentric and the other is normal,
of course half of the gametes would likely be aberrant.
> In
> Drosophila, OTOH, dicentric chromatids do not break and typically wind
> up in the polar bodies rather than the egg. And produce ineffective
> double-headed sperm. So the aberrations do not reach the stage of
> being in the gametes, whereas the chromatids not involved in crossing
> over do get into functional sperm and egg.
There is still a reduction in normal gamete production. The offspring
would be normal in such a situation - both viable and fertile.
This is completely irrelevant to the reason why breeding between some
creatures, like donkeys and horses, produce viable, but not fertile
offspring.
> Meioses in which there has been no intra-inversion crossing over
> produce perfectly normal eggs and sperm in perfectly normal amounts.
That's right.
> The reduction in fertility, then, is a lot less than one might expect
> *unless* there are multiple or very large inversions.
Why would one expect a significant reduction in hybrid fertility
unless there are multiple or large inversions? Who is suggesting
otherwise here?
> Significant
> reduction in fertility often requires multiple chromosome
> rearrangement, not just one.
Only one is required if it is large or in a place of prominent
crossover events. Of course, multiple inversions would increase the
odds of hybrid infertility.
> BTW, there are multiple rearrangement differences between humans and
> chimp, but as the mule (and the more pathetic hinny) shows, that does
> not prevent viability of the hybrid.
Exactly . . .
> For the reason why humans and
> chimps do not produce viable hybrids, you have to look elsewhere.
LOL - Right. The reason is obviously that there is an informational
disconnect between humans and chimps that is not present between
horses and donkeys. The genetic information of the chimp is telling
the growing embryo to do one thing while the information of the human
is telling the embryo to do another. The conflicting orders result in
a non-viable embryo.
> > So, the mule cannot make egg or
> > sperm cells. Thus, the mule is sterile. However, a mule can still be
> > born healthy because such growth of non-meiotic cells occurs via a
> > different process called mitosis. Mitosis does not have to match
> > things up; it only has to make copies. So, inversions and
> > translocations do not prevent the mule from growing up to be an adult.
>
> > Perhaps a little refresher course in genetics is in order?
>
> Yes. You do need to take one.
LOL - I've taken many. What you need to do is to try to stick on
topic instead of throwing around a bunch of irrelevant red herrings.
> >http://www.detectingdesign.com/donkeyshorsesmules.html
>
> > > So your entire assumption (interfertility
> > > equals identity of "genetic information") is just a BS assumption on
> > > yourn part that you can't demonstrate in any way whatsoever.
>
> > You just don't understand the genetics involved.
>
> > > You've still not answered the most basic elementary of questions: How
> > > do you measure this "distance in sequence space", and how can you
> > > therefore show that humans and chimps are further apart in it than any
> > > other two species are.
>
> > I've already told you several times. You can know that they are
> > likely further, but by how much is not knowable yet.
>
> What we know is that there is no sequence difference in any gene or
> even any length of DNA sequence between chimps and humans that is
> unaccountable for by the known rates of change that can be permitted
> by selection for change.
Not true. There are lots of unique miRNAs and other non-coding
elements between humans and chimps that collectively represent a
sizable percentage of the total genome. How these non-coding elements
interplay to produce end-structure differences that are potentially
quite significant in both structural and functional uniqueness is not
completely understood. Therefore, it cannot be said that
significantly complex functional differences do not exist in a
qualitative manner.
> In fact, there are almost no genes or
> lengths of DNA with more change than would be expected by neutral
> drift from a common ancestor in the time available. There is nothing
> in the amount of change in DNA sequences between human and chimp that
> requires non-natural or exceptionally rapid intervention by an outside
> agent, intelligent or otherwise.
You don't have enough information to make this claim. The functional
differences and the underlying genetics upon which these are based are
not adequately understood yet.
> > You know that
> > they are further because they cannot produce viable much less fertile
> > offspring. Try to remember this time.
>
> In the case of human and chimp, the reason for inviability of hybrids
> would most likely lie in differences in rates of development of
> various organs leading to early lethality due to developmental
> discord. It would not be due to chromosomal rearrangements.
You've just made my point for me. The lack of hybrid viability is not
due to chromosomal rearrangements, but is most likely do to
incompatible informational differences between the genomes. Again, my
entire argument is that informational differences, qualitative
informational differences, are what should be used to define species
in a more objective manner. As it currently stands, species are not
defined by unique qualitative genetic differences, but often
quantitative genetic differences. That is why the term "species" is
so subjective as to be hardly useful in science at all.
Sean Pitman
www.DetectingDesign.com
seanpi...@naturalselection.0catch.com
> On Dec 2, 10:10 pm, Seanpit <sean...@gmail.com> wrote:
>
>
>
> > Great - please detail exactly where I went wrong in my thinking . . .
>
> What "thinking"? All I've seen from you is "there's no current
> genetic reason to say that humans and chimps are not related by
> descent, but I think they are because of a, uh, unknown measurement
> that I can't describe or measure."
You're the one who thinks that creatures that can at least produce
viable and occasionally fertile offspring are more distantly "related"
than those that can't produce viable much less fertile offspring. Go
figure . . .
You don't need to have a specific known measure of the distance to
suspect that perhaps, just perhaps, the combo that can't produce a
viable much less a fertile offspring is informationally more
incompatible compared to the combo that can produce viable and
occasionally fertile offspring.
Is more information needed? Certainly would be helpful. Is it
available yet? Nope, not yet. So, what is the best available evidence
telling us? How far can you go with what we have? Upon what basis do
you declare that humans and chimps are obviously more closely related
than horses and donkeys? - sequence comparisons of certain selected
kinds of DNA sequences? That's it? Pretty subjective if you ask me.
You don't even consider the functional aspects of the genome at all.
You really think you can adequately determine "relationships" based on
pattern analysis alone? - without considering any evidence regarding
the functional differences of the different genomes or genetic regions
in question? Amazing . . .
> BFD.
>
> Why don't you just post some quotes from Henry Morris declaring that
> "new genetic information can't appear randomly". That's shorter to
> say, easier to remember, and was already demonstrated to be bullshit
> twenty years ago, so it saves everybody's time. (shrug)
New genetic information can appear via random mechanisms. It happens
all the time very rapidly and very commonly. It just doesn't happen
beyond very low levels of functional complexity. There is an
observable limit to evolutionary progress via the mechanism of RM/NS.
There is also an observable stalling out effect that is exponential in
nature. That's the problem.
>
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
> Editor, Red and Black Publishershttp://www.RedandBlackPublishers.com
Sean Pitman
www.DetectingDesign.com
hersheyh
Depends on the number of crossovers within the inversion. If there is
only one crossover, then only two of the chromatids are affected.
Hence one half. If there are two or more, then what we get depends
upon whether there are two, three, or four strand events.
For a simple understanding of the consequences, see:
http://www.med.nyu.edu/sackler/genetic/Translocations_and_Invers.htm
> > *In
> > practice* it depends on the species. In corn, for example, dicentric
> > chromosomes break, leading to the possibility of an egg getting an
> > aberrant chromosome (and half of pollen getting aberrations).
>
> Dicentric chromosomes aren't the same thing as chromosomal
> inversions. If one chromosome is dicentric and the other is normal,
> of course half of the gametes would likely be aberrant.
When you have a paracentric inversion and a crossover within that
inversion, you generate both an acentric fragment that gets lost and a
dicentric chromosome that either gets trapped or gets broken.
See:
http://www.med.nyu.edu/sackler/genetic/Translocations_and_Invers.htm
With really complex inversion, crossing over is actually suppressed
within the inverted region.
> > In
> > Drosophila, OTOH, dicentric chromatids do not break and typically wind
> > up in the polar bodies rather than the egg. And produce ineffective
> > double-headed sperm. So the aberrations do not reach the stage of
> > being in the gametes, whereas the chromatids not involved in crossing
> > over do get into functional sperm and egg.
>
> There is still a reduction in normal gamete production. The offspring
> would be normal in such a situation - both viable and fertile.
Yes. And the loss in fertility often would be small because the
capacity to produce sperm and eggs far outstrips the number that get
used or survive. After all, in the evening primrose, which has
multiple translocations producing ring chromosomes at meiosis, half of
the fertilized zygotes die early in development.
> This is completely irrelevant to the reason why breeding between some
> creatures, like donkeys and horses, produce viable, but not fertile
> offspring.
>
> > Meioses in which there has been no intra-inversion crossing over
> > produce perfectly normal eggs and sperm in perfectly normal amounts.
>
> That's right.
>
> > The reduction in fertility, then, is a lot less than one might expect
> > *unless* there are multiple or very large inversions.
>
> Why would one expect a significant reduction in hybrid fertility
> unless there are multiple or large inversions? Who is suggesting
> otherwise here?
All you said was:
*******
> > > For example, if a piece of donkey chromosome is inverted relative to
> > > its counterpart in horses, then gene-by-gene pairing cannot occur
> > > without elaborate looping and twisting. The chance of a successful
> > > cell division is very much reduced.
*******
No mention, even, of the requirement that there be crossing over, much
less that there be *multiple* rearrangements.
> > Significant
> > reduction in fertility often requires multiple chromosome
> > rearrangement, not just one.
>
> Only one is required if it is large or in a place of prominent
> crossover events. Of course, multiple inversions would increase the
> odds of hybrid infertility.
>
> > BTW, there are multiple rearrangement differences between humans and
> > chimp, but as the mule (and the more pathetic hinny) shows, that does
> > not prevent viability of the hybrid.
>
> Exactly . . .
>
> > For the reason why humans and
> > chimps do not produce viable hybrids, you have to look elsewhere.
>
> LOL - Right. The reason is obviously that there is an informational
> disconnect between humans and chimps that is not present between
> horses and donkeys. The genetic information of the chimp is telling
> the growing embryo to do one thing while the information of the human
> is telling the embryo to do another. The conflicting orders result in
> a non-viable embryo.
But such disconnect does not necessarily require massive changes in
the genome. It can occur because of a single mutational difference.
Do you know of any *qualitative* phenotypic difference between humans
and chimps? I don't. I see lots of *quantitative* differences. And
a fossil record that shows some of the intermediate quantitative
stages in the transition, say between a chimp and human cephalic index
or degrees of bipedality.
So now you are imagining or positing complex functional differences
that are qualitative in nature without the slightest evidence *at the
phenotypic level that we can actually observe* that there is such a
thing? Sort of like your imagining bacteria that include total
sequence space within their teeny little bodies.
Come on. Give me an example of what you mean by a *qualitative*
phenotypic difference between humans and chimps. And why that
*qualitative* difference requires the instantaneous spontaneous change
in all the miRNAs.
The fact remains that the *quantitative* amount of difference between
humans and chimps is mostly selectively neutral with only a few places
where there is a need to invoke selection. And the fossil record is
not one of qualitative intermediates, but only of quantitative
intermediates. I see no reason to invoke the unlikely idea that for
some un-named and apparently invisible and unobserved qualitative
phenotypic difference that one must have a thousand instantaneous
mutations in a whole bunch of *regulatory* elements. Call me when you
have a candidate. Until then all you have is a hopeful wish without
even the supporting evidence of a potential candidate phenotype.
> > In fact, there are almost no genes or
> > lengths of DNA with more change than would be expected by neutral
> > drift from a common ancestor in the time available. There is nothing
> > in the amount of change in DNA sequences between human and chimp that
> > requires non-natural or exceptionally rapid intervention by an outside
> > agent, intelligent or otherwise.
>
> You don't have enough information to make this claim.
Sure I do. I said that there is nothing in the *amount* of change in
DNA sequences that requires non-natural or exceptionally rapid
intervention by an outside agent. You are positing that *hidden
within* this *amount* of change that could occur naturally there might
possibly be some unknown qualitative phenotypic difference that
required the simultaneous, but individually small, change in a
thousand (or whatever) miRNAs. This is claimed without your being able
to specify even a possible example of a qualitative phenotypic
difference between humans and chimps. It isn't like one cannot
observe these organisms.
> The functional
> differences and the underlying genetics upon which these are based are
> not adequately understood yet.
Any examples of qualitative differences that do not amount to wishful
thinking?
> > > You know that
> > > they are further because they cannot produce viable much less fertile
> > > offspring. Try to remember this time.
>
> > In the case of human and chimp, the reason for inviability of hybrids
> > would most likely lie in differences in rates of development of
> > various organs leading to early lethality due to developmental
> > discord. It would not be due to chromosomal rearrangements.
>
> You've just made my point for me. The lack of hybrid viability is not
> due to chromosomal rearrangements, but is most likely do to
> incompatible informational differences between the genomes.
Yes.
> Again, my
> entire argument is that informational differences, qualitative
> informational differences, are what should be used to define species
> in a more objective manner. As it currently stands, species are not
> defined by unique qualitative genetic differences, but often
> quantitative genetic differences. That is why the term "species" is
> so subjective as to be hardly useful in science at all.
What you mean is that the reality of species and speciation do not fit
your religious ideology.
>
> Sean Pitmanwww.DetectingDesign.com
Mark Isaak
> On 3 Dec, 15:57, Mark Isaak <eci...@earthlink.net> wrote:
>> On Tue, 02 Dec 2008 19:04:48 -0800, Seanpit wrote:
>> >[snip]
>> > Fertility isn't an informational problem as much as it is a
>> > chromosomal structural problem.
>>
>> Fertility is a fertility problem. A single mutation in a specific
>> compatibility gene can cause infertility; a million mutations and
>> chromosome rearrangements in other genes can leave things fertile.
>
> What's a "compatibility gene"?
A gene which regulates reproductive compatibility.
Seanpit
wrote:
It is fine to have your "reasons". It is just that not everyone in
mainstream science agrees with you on this one. Of course, that's
fine. Obviously, most in mainstream science don't agree with me on
many ideas that I think are perfectly "reasonable".
So, anyway, add me to the list of those who don't think your reasons
are reasonable in this particular case. You can't just discount
insertions or deletions of DNA in one genome relative to another as
obviously being informationally irrelevant when we know that more and
more these very same differences are actually functional - and
possibly uniquely functional on an individual or collective basis.
After all, based just on mutational differences alone, regardless of
the size of the difference, modern humans can be just as distantly
"related" as humans and chimps - yet these modern humans can can still
interbreed to produce viable and fertile offspring.
"With the decoding of complete human genome, scientists have now
concluded that we are not as similar genetically as we thought we
were: people share perhaps 99 per cent, rather than 99.9 per cent, of
their genes."
Indian J Physiol Pharmacol 2008; 52(2) : 103–105
http://www.ijpp.com/vol52_2/103-105.pdf
This discrepancy is likely due to the fact that mutation rates in
human genomes are far greater than previously though - by an order of
magnitude.
"The mean µ in cells from normal donors was 10.6 x 10^–7
mutations per cell division (range 2.4 to 29.6 x 10^–7)."
http://cancerres.aacrjournals.org/cgi/content/full/65/18/8111
See also: http://www.nature.com/nature/journal/v430/n7000/full/nature02697.html
Clearly then, the argument of clear species delineation based only on
the gross numbers of genetic differences without any regard to the
quality of those differences is a gross oversimplification of the
concept of "relationships" between different living things.
> >>> The author of one such study, Roy J. Britten, argues:
> >>> "It appears appropriate to me to consider the full length of the
> >>> gaps in estimating the interspecies divergence. These stretches of DNA
> >>> are actually absent from one and present in the other genome. In the
> >>> past, indels have often simply been counted regardless of length and
> >>> added to the base substitution count, because that is convenient for
> >>> phylogenetics."
> >> Yes, and I think Britten's idea is silly. What biological reason is
> >> there to count the lengths of gaps, when each gap is generally a single
> >> mutation? A 1-base gap is 1 mutation; a thousand-base gap is 1 mutation.
>
> > A difference of 1000 bp could be functionally significant - regardless
> > of how it was produced. That is why Britten's method makes much more
> > sense than only counting non-gap regions of DNA.
>
> What makes the most sense is counting mutations. Humans and chimps
> differ by 40 million mutations. 35 million of those are point
> substitutions. 5 million are indels. There are a negligible few more
> that don't fall into either category, such as chromosomal fusions,
> inversions, and perhaps a few more categories I'm not thinking of.
Yeah - and modern humans can have this many individual mutational
differences with the next-door neighbor when it comes to absolute
numbers when one isn't concerned about the quality of the difference
(i.e., size and/or functional features).
> A difference of 1000bp could be functionally significant, and so could a
> single point substitution. So?
That's the really important question. That's what isn't adequately
known at this point. The only thing that is clear is that there is a
clearly difference in viable hybrid production.
> I'm not saying you should count only
> non-gap regions. I'm saying you should count one mutation as one
> mutation. A 10-base indel is not any more or less a single mutation than
> a 1000-base indel.
It could be more or less functionally important. That's what you're
"method" doesn't consider.
> >>> Britten, R.J., Divergence between samples of chimpanzee and human DNA
> >>> sequences is 5%, counting indels, Proc. Nat. Acad. Sci. USA 99(21):
> >>> 13633–13635, 2002.
> >>> His findings lend support to the idea that much of the failure of DNA
> >>> to hybridize between chimps and humans is the result of missing DNA
> >>> due to indel events.
> >> What failure to hybridize are you talking about here? Perhaps you mean
> >> that most sequences that don't hybridize are those that are not shared.
> >> That makes sense, as the other reason for having a non-hybridized
> >> fraction in a DNA-DNA hybridization experiment is high sequence
> >> divergence, which isn't going to happen between humans and chimps.
>
> > Exactly . . .
>
> So?
>
> >>> Britten then became involved in a follow-up paper in which these
> >>> initial results were confirmed; in fact, it was found that "the 5%
> >>> human-chimp difference already published is likely to be an
> >>> underestimate, possibly by more than a factor of 2." - - in other
> >>> words by more than 10%.
> >>
> >> Again, the estimate is biologically meaningless.
>
> > How do you know? . . .
>
> Explain its biological meaning.
The meaning is a potential meaning. We just don't know enough yet.
However, the potential biological meaning cannot be dismissed out of
hand either - like you are trying to do. You simply do not know
enough to adequately say, "The estimate is biologically meaningless."
At best you can say that you just don't know if there or isn't a
significant biological meaning. Beyond this, there does seem to be a
significant biological meaning given the fact that no viable much less
fertile hybrids can be produced. It is also likely that such
differences explain certain key structural and functional differences
as well - like those seen in the brain down to the cellular level.
That's right.
> I don't
> know your definition of information, so can't be sure what you meant to
> say. I just point out that your initial assertion about the nature of
> that 98.5% similarity is wrong, based on what you yourself have quoted.
It isn't wrong. And, my definition of functional informational
complexity is quite clear - a system of beneficial function that
requires at least a certain size and specificity minimum.
That's what I'm saying. It depends upon what region or type of DNA
you're dealing with. If you dealing with a region that is especially
important in governing the production of a significant phenotypic
difference, you're going to get a greater genetic difference as well.
This is why doing it your way is essentially meaningless. You way
could be used put certain groups of modern humans under different
species classifications. It is scientifically meaningless as you
apply it.
The fact that a particular system requires multiple genetic elements
to produce it is not in question here. A flagellar system requires at
minimum dozens of individual "genes" to produce it. This is a fact
regardless of how these individual genes were produced. Now, you
think they were produced by RM/NS. You believe this without any
demonstration of the production of any novel system of function that
requires at least 1000 fsaars. You also have no statistical basis for
this belief of yours. You have nothing but just-so stories. That's
it. That's not science. The very same thing is potentially true when
it comes to systems that are based on the input of multiple miRNAs.
> >>>> [snip Sean's "baffle with bullshit" phase]
> >>> What? You think the fact that humans and apes do not produce viable
> >>> much less fertile offspring is irrelevant?
> >> Yes. Some closely related species can't produce viable offspring. Some
> >> distantly related species can. There is no particular correlation
> >> between closeness of relationship and hybridization.
>
> > Ah, care to provide some actual examples?
>
> The problem with this is that I don't know what you are willing to
> consider related, since I have no idea what a "kind" is supposed to be.
> But this is a commonplace fact of science.
Only by your personal definition of genome "relationships".
> > I say that there is a very good correlation between qualitative
> > functional aspects of a gene pool and hybridization. Allelic
> > variations with the same qualitative function aren't in question
> > here. Many quantitative differences can exist between gene pools -
> > just as long as the qualitative functional features and options are
> > the same.
>
> That's fine for you, because the undefined nature of "qualitative
> functional features and options", being known only to you, makes it
> possible for you to ignore any examples I might bring out.
>
> But let's try. Does the entire family Anatidae share all the same
> qualitative functions?
I don't know about "all", since these sorts of things are often
subjectively determined. However, I would say that many members of
Anatidae family do share the same essential gene pool.
Swan-Goose hybrid:
http://elibrary.unm.edu/sora/Auk/v045n01/p0039-p0040a.pdf
Domestic Duck x Domestic Goose hybrid:
http://en.wikipedia.org/wiki/Bird_hybrid
> >>> How is the presentation of
> >>> examples of interbreeding species that produce at least viable and
> >>> even occasionally fertile offspring at all germane when it comes to
> >>> the argument that humans and chimps are even more closely related?
> >> It isn't. Nor is the inability of chimps and humans to hybridize.
>
> > Think again. One of the very foundations of the concept of
> > "speciation" involves the ability to successful mate and interbreed.
>
> That was a bizarre non sequitur, and I have no idea how to respond.
>
> > This means producing both viable and fertile offspring. If at least
> > the viability part of this equation is intact in one pairing, but not
> > another, which pairing most likely represents a more functionally
> > "close" or "similar" pairing?
>
> I have no idea, since none of your terms are defined. How do we
> determine functional similarity?
You have to know something about the actual functional systems in both
creatures in question. This is not yet know to an adequate degree for
either humans or chimps. All that is known is that there is very
likely some significant functional differences due to the fact that
viable hybrids are not produced.
> >>> even though they cannot produce viable much less fertile offspring?
> >>> Who's BSing here?
> >> You are, as I've already mentioned several times.
>
> > LOL - right ; )
>
> Thanks for admitting that, at least.
Only someone as arrogant as you would interpret this as an admission.
You have to know that I think you are way off base in just about
everything you say. You're arguments are strained and confused and I
think many are throw out there just to see if they will fly - like a
bunch of BS. But hey, you stick to your guns and you say it like you
see it. I like that about you. I think you're at least genuinely
honest in your beliefs - - for the most part.
Sean Pitman
www.DetectingDesign.com
hersheyh
> On 2 Dec, 22:16, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
> > On Dec 2, 10:10 pm, Seanpit <sean...@gmail.com> wrote:
>
> > > Great - please detail exactly where I went wrong in my thinking . . .
>
> > What "thinking"? All I've seen from you is "there's no current
> > genetic reason to say that humans and chimps are not related by
> > descent, but I think they are because of a, uh, unknown measurement
> > that I can't describe or measure."
>
> You're the one who thinks that creatures that can at least produce
> viable and occasionally fertile offspring are more distantly "related"
> than those that can't produce viable much less fertile offspring. Go
> figure . . .
And, in fact, the degree of reproductive isolation is only very
loosely correlated with the degree of *genetic* relatedness. Degree of
genetic relatedness is determined by the amount of genetic difference
between two species or organisms. The degree of reproductive
isolation, OTOH, is a function of specific genetic differences, those
that affect reproduction not surprisingly.
> You don't need to have a specific known measure of the distance to
> suspect that perhaps, just perhaps, the combo that can't produce a
> viable much less a fertile offspring is informationally more
> incompatible compared to the combo that can produce viable and
> occasionally fertile offspring.
Not true. Think polyploid species. Reproductive isolation is due to
*specific* types of variation. There are highly genetically variable
species. And there are nearly indistinguishable species that are
reproductively isolated from each other. In fact, both genetic
variability and reproductive isolation can occur within a species.
For example, northern Rana pipiens (frogs) cannot produce offspring
with southern Rana pipiens because both populations are adapted to
development in different water conditions (mainly temperature) and
hybrid offspring have lethal developmental abnormalities because of
the 'conflict' between genes and optimal water temperature for
development. But there are frogs in the intermediate areas that allow
gene flow.
>
> Is more information needed? Certainly would be helpful. Is it
> available yet? Nope, not yet. So, what is the best available evidence
> telling us? How far can you go with what we have? Upon what basis do
> you declare that humans and chimps are obviously more closely related
> than horses and donkeys? - sequence comparisons of certain selected
> kinds of DNA sequences? That's it? Pretty subjective if you ask me.
> You don't even consider the functional aspects of the genome at all.
> You really think you can adequately determine "relationships" based on
> pattern analysis alone? - without considering any evidence regarding
> the functional differences of the different genomes or genetic regions
> in question? Amazing . . .
I frankly do not know the mean genetic difference between horse and
donkey and whether that is greater or smaller than the mean genetic
difference between human and chimp. But the mechanism of reproductive
isolation is probably different, since I know that horse-donkey
hybrids are viable but sterile (one type of reproductive isolation)
and human-chimp hybrids are apparently not viable (I am not quite sure
of the mechanism; it could be gamete incompatibility or failure of
sperm from one species to fertilize an egg of the other or it could be
developmental incompatibility or it could be simple repugnance).
John Harshman
> On 3 Dec, 20:50, hersheyh <hershe...@yahoo.com> wrote:
>> In the case of human and chimp, the reason for inviability of hybrids
>> would most likely lie in differences in rates of development of
>> various organs leading to early lethality due to developmental
>> discord. It would not be due to chromosomal rearrangements.
>
> You've just made my point for me. The lack of hybrid viability is not
> due to chromosomal rearrangements, but is most likely do to
> incompatible informational differences between the genomes. Again, my
> entire argument is that informational differences, qualitative
> informational differences, are what should be used to define species
> in a more objective manner. As it currently stands, species are not
> defined by unique qualitative genetic differences, but often
> quantitative genetic differences. That is why the term "species" is
> so subjective as to be hardly useful in science at all.
Let's put species on the list of things Sean doesn't know much about.
Species are not defined by quantitative genetic differences. Species are
defined (at least "biological" species, the most common meaning) by the
existence of some isolating mechanism that prevents large-scale
introgression between populations. Note that hybrids between species may
be perfectly viable and perfectly fertile, as long as there is some
selective disadvantage that prevents much gene flow. Under the
phylogenetic species concept, no genetic isolating mechanism is
necessary if the populations are geographically separated and there is
therefore no gene flow.
Now if there are large quantitative genetic differences between
populations, one has a reason to expect that there might be a reason for
those differences, presumably a lack of significant gene flow, and
depending on your species concept you might suppose they are different
species. But genetic difference isn't the criterion, merely a clue.
One of which you should get.
John Harshman
I don't know what you mean by "informationally irrelevant". Nor do I
suggest discounting indels. I just think counting each base of an indel
as a separate difference, equivalent in value to a base substitution, is
silly. If you're going to count, count mutations.
> After all, based just on mutational differences alone, regardless of
> the size of the difference, modern humans can be just as distantly
> "related" as humans and chimps - yet these modern humans can can still
> interbreed to produce viable and fertile offspring.
Even if you put "related" in quotes, that isn't true.
> "With the decoding of complete human genome, scientists have now
> concluded that we are not as similar genetically as we thought we
> were: people share perhaps 99 per cent, rather than 99.9 per cent, of
> their genes."
What does this actually mean? As written, it makes no sense.
> Indian J Physiol Pharmacol 2008; 52(2) : 103–105
> http://www.ijpp.com/vol52_2/103-105.pdf
>
> This discrepancy is likely due to the fact that mutation rates in
> human genomes are far greater than previously though - by an order of
> magnitude.
So you may believe. But why are you going off on this odd tangent? Is it
just that we have come within attraction range of one of your obsessions?
> "The mean µ in cells from normal donors was 10.6 x 10^–7
> mutations per cell division (range 2.4 to 29.6 x 10^–7)."
>
> http://cancerres.aacrjournals.org/cgi/content/full/65/18/8111
>
> See also: http://www.nature.com/nature/journal/v430/n7000/full/nature02697.html
>
> Clearly then, the argument of clear species delineation based only on
> the gross numbers of genetic differences without any regard to the
> quality of those differences is a gross oversimplification of the
> concept of "relationships" between different living things.
Agreed. That's why nobody uses the gross numbers of genetic differences
to delineate species. It's another of your strawmen. Again, I'm not sure
what you mean by "relationships", in quotes.
>>>>> The author of one such study, Roy J. Britten, argues:
>>>>> "It appears appropriate to me to consider the full length of the
>>>>> gaps in estimating the interspecies divergence. These stretches of DNA
>>>>> are actually absent from one and present in the other genome. In the
>>>>> past, indels have often simply been counted regardless of length and
>>>>> added to the base substitution count, because that is convenient for
>>>>> phylogenetics."
>>>> Yes, and I think Britten's idea is silly. What biological reason is
>>>> there to count the lengths of gaps, when each gap is generally a single
>>>> mutation? A 1-base gap is 1 mutation; a thousand-base gap is 1 mutation.
>>> A difference of 1000 bp could be functionally significant - regardless
>>> of how it was produced. That is why Britten's method makes much more
>>> sense than only counting non-gap regions of DNA.
>> What makes the most sense is counting mutations. Humans and chimps
>> differ by 40 million mutations. 35 million of those are point
>> substitutions. 5 million are indels. There are a negligible few more
>> that don't fall into either category, such as chromosomal fusions,
>> inversions, and perhaps a few more categories I'm not thinking of.
>
> Yeah - and modern humans can have this many individual mutational
> differences with the next-door neighbor when it comes to absolute
> numbers when one isn't concerned about the quality of the difference
> (i.e., size and/or functional features).
What do you mean by "this many"? Are you claiming that next-door
neighbors can differ by as many as 40 million mutations? Show me some
evidence for that claim, if so.
>> A difference of 1000bp could be functionally significant, and so could a
>> single point substitution. So?
>
> That's the really important question. That's what isn't adequately
> known at this point. The only thing that is clear is that there is a
> clearly difference in viable hybrid production.
What is your point, if any?
>> I'm not saying you should count only
>> non-gap regions. I'm saying you should count one mutation as one
>> mutation. A 10-base indel is not any more or less a single mutation than
>> a 1000-base indel.
>
> It could be more or less functionally important. That's what you're
> "method" doesn't consider.
Nor does any method so far devised. What is your point?
Yes I do. And so do you. You just like that estimate because it inflates
the amount of difference, and you want to emphasize differences. You
could achieve the same effect by multiplying by 10, with as much
biological meaning. A thousand-base indel is not much more likely to be
functionally more important than a one-base indel. Even if you're
looking for some measure of functional genetic difference, Britten's
measure is no more similar to such a measure than is counting only
mutations or homologous base differences.
> At best you can say that you just don't know if there or isn't a
> significant biological meaning. Beyond this, there does seem to be a
> significant biological meaning given the fact that no viable much less
> fertile hybrids can be produced. It is also likely that such
> differences explain certain key structural and functional differences
> as well - like those seen in the brain down to the cellular level.
Here you seem to have abandoned the distance measure entirely and gone
off into your own obsession. As I said, functional difference is not
strongly correlated with genetic distance, by any of the measures so far
proposed. You may imagine some kind of functional genetic distance
measure, but there is none, at least yet. No matter how much you want to
imagine one.
If that's what you mean, why can't you just say it?
>> I don't
>> know your definition of information, so can't be sure what you meant to
>> say. I just point out that your initial assertion about the nature of
>> that 98.5% similarity is wrong, based on what you yourself have quoted.
>
> It isn't wrong.
Yes it is. Let's review. You said "This 98.5% number is usually based on
homologies of protein-coding genes." Remember now?
> And, my definition of functional informational
> complexity is quite clear - a system of beneficial function that
> requires at least a certain size and specificity minimum.
It's operationally useless, and completely unclear. It's unquantifiable,
and I bet no two people would come up with the same estimate.
Then why did you say what you said? Do you even remember what you write
from one post to the next?
> It depends upon what region or type of DNA
> you're dealing with. If you dealing with a region that is especially
> important in governing the production of a significant phenotypic
> difference, you're going to get a greater genetic difference as well.
> This is why doing it your way is essentially meaningless. You way
> could be used put certain groups of modern humans under different
> species classifications. It is scientifically meaningless as you
> apply it.
Sorry, too many ambiguous referents here. You seem incapable of clear
writing. I don't know what "my way" is, or how it could be used to split
humans into multiple species. (Incidentally, you still seem to be
laboring under the delusion that species limits are determined by
genetic distance.) I don't know what I'm claimed to be applying or why.
Or what a "region" is, or what is expected to show greater genetic
difference.
Yes it is. You claim that the human brain must have emerged fully formed
at the creation, because there can be no functional intermediates
between an ape brain and a modern human brain. That's your whole
argument, such as it is.
> A flagellar system requires at
> minimum dozens of individual "genes" to produce it. This is a fact
> regardless of how these individual genes were produced. Now, you
> think they were produced by RM/NS. You believe this without any
> demonstration of the production of any novel system of function that
> requires at least 1000 fsaars. You also have no statistical basis for
> this belief of yours. You have nothing but just-so stories. That's
> it. That's not science. The very same thing is potentially true when
> it comes to systems that are based on the input of multiple miRNAs.
I know flagella are one of your obsessions, but try to stay on track
here. You have no evidence for the "irreducible complexity" of the set
of miRNAs you're looking at, or of the human brain.
>>>>>> [snip Sean's "baffle with bullshit" phase]
>>>>> What? You think the fact that humans and apes do not produce viable
>>>>> much less fertile offspring is irrelevant?
>>>> Yes. Some closely related species can't produce viable offspring. Some
>>>> distantly related species can. There is no particular correlation
>>>> between closeness of relationship and hybridization.
>>> Ah, care to provide some actual examples?
>> The problem with this is that I don't know what you are willing to
>> consider related, since I have no idea what a "kind" is supposed to be.
>> But this is a commonplace fact of science.
>
> Only by your personal definition of genome "relationships".
It's the standard definition. Relationships are genealogical. Ancestors.
Descendants. Your genome is related to mine through descent with
modification. On that we agree. Your genome and mine are related to
those of chimps in exactly the same way. On that you disagree, but don't
claim it's my personal definition rather than the standard scientific
definition. And again you haven't helped; I still don't know what a
"kind" is.
>>> I say that there is a very good correlation between qualitative
>>> functional aspects of a gene pool and hybridization. Allelic
>>> variations with the same qualitative function aren't in question
>>> here. Many quantitative differences can exist between gene pools -
>>> just as long as the qualitative functional features and options are
>>> the same.
>> That's fine for you, because the undefined nature of "qualitative
>> functional features and options", being known only to you, makes it
>> possible for you to ignore any examples I might bring out.
>>
>> But let's try. Does the entire family Anatidae share all the same
>> qualitative functions?
>
> I don't know about "all", since these sorts of things are often
> subjectively determined. However, I would say that many members of
> Anatidae family do share the same essential gene pool.
>
> Swan-Goose hybrid:
> http://elibrary.unm.edu/sora/Auk/v045n01/p0039-p0040a.pdf
>
> Domestic Duck x Domestic Goose hybrid:
> http://en.wikipedia.org/wiki/Bird_hybrid
Talk about begging the question! You ask me to provide evidence of
hybridization between species with different qualitative functional
features, yet you consider the mere fact of hybridization to be
conclusive evidence of a lack of such differences! It's therefore
impossible for me to present an example, by definition. Do you
understand how your reasoning is hermetically circular?
I agree with you that the judgment is subjective; but of course that
makes it operationally useless.
Ducks and geese have huge genetic distances, by the way, much much more
than that between humans and chimps by any measure you care to try.
>>>>> How is the presentation of
>>>>> examples of interbreeding species that produce at least viable and
>>>>> even occasionally fertile offspring at all germane when it comes to
>>>>> the argument that humans and chimps are even more closely related?
>>>> It isn't. Nor is the inability of chimps and humans to hybridize.
>>> Think again. One of the very foundations of the concept of
>>> "speciation" involves the ability to successful mate and interbreed.
>> That was a bizarre non sequitur, and I have no idea how to respond.
>>
>>> This means producing both viable and fertile offspring. If at least
>>> the viability part of this equation is intact in one pairing, but not
>>> another, which pairing most likely represents a more functionally
>>> "close" or "similar" pairing?
>> I have no idea, since none of your terms are defined. How do we
>> determine functional similarity?
>
> You have to know something about the actual functional systems in both
> creatures in question. This is not yet know to an adequate degree for
> either humans or chimps. All that is known is that there is very
> likely some significant functional differences due to the fact that
> viable hybrids are not produced.
Again, begging the question. You asked me to provide an example of
hybridization despite functional differences, or lack of hybridization
despite no functional differences, but your sole evidence for such
differences is lack of hybridization.
>>>>> even though they cannot produce viable much less fertile offspring?
>>>>> Who's BSing here?
>>>> You are, as I've already mentioned several times.
>>> LOL - right ; )
>> Thanks for admitting that, at least.
>
> Only someone as arrogant as you would interpret this as an admission.
Only someone as clueless as you would require a smiley to understand irony.
> You have to know that I think you are way off base in just about
> everything you say. You're arguments are strained and confused and I
> think many are throw out there just to see if they will fly - like a
> bunch of BS.
For the record, I never do that.
> But hey, you stick to your guns and you say it like you
> see it. I like that about you. I think you're at least genuinely
> honest in your beliefs - - for the most part.
And I don't think you are. I think you're a biblical literalist who is
merely pretending it's all about the science, nothing more. Perhaps you
conceal this from yourself and so can be considered in some sense
sincere. But you're lying to somebody.
'Rev Dr' Lenny Flank
> You don't need to have a specific known measure of the distance to
> suspect that perhaps, just perhaps, the combo that can't produce a
> viable much less a fertile offspring is informationally more
> incompatible compared to the combo that can produce viable and
> occasionally fertile offspring.
You have nothing whatever to justify the assumotion that
"interfertility is a measure of genetic distance".
None.
Not a shred.
Zip.
Zero.
Zilch.
Not surprising, though, since you can't even tell us what the hell
"genetic distance" (or "gap in sequence space") IS, much less how we
can tell which species are closer in "sequence space" and which are
further apart . . . . .
'Rev Dr' Lenny Flank
>There is an
> observable limit to evolutionary progress via the mechanism of RM/NS.
Really. . . .
What.
What is this "limit", how is it produced, and what mechanism is it
that allows genetic changes to happen within this "limit" but prevents
any genetic changes from crossing this "limit"?
'Rev Dr' Lenny Flank
wrote:
(snip)
> I don't know what you mean by "informationally irrelevant".
Indeed, thirty years ago, when creation "scientists" were blithering
that "genetic information can't increase", THEY couldn't tell anyone
what the hell they meant by "genetic information" either, or how to
measure it.
And neither can Sean.
'Rev Dr' Lenny Flank
wrote:
But he's also arguing that the fact that humans are closer to chimps,
genetically, than other species, doesn't mean they are closer in
"sequence space" (whatever the hell THAT means) than other species.
So he is indeed making a claim about sequence space and its similarity
(or lack of) between species.
The problem though is that he's just talking out his ass, since he
can't even tell us what this "gap in sequence space" IS, much less how
to measure it -- or why it's a beter measure than similarity of DNA.
Iit seems a reasonable assumption to me that (with all the standard
caveats and pitfalls) the more similar the DNA of two species is, the
more closely related they are. That, after all, is how plain old
ordinary standard DNA paternity testing and ancestry-tracing is done,
and it seems to work just fine and dandy. . . . And it also has the
advantage of being an objective measurement that anyonhe can
understand and perform, unlike Sean's "gaps in sequence space".
Sean is of course entirely free to reject all that, since it conflicts
with his religious opinions. But then, in the real world, nobody
cares what Sean accepts or rejects anyway. Since the entire
creationist political movement is now dead as a mackerel, the claims
of that movement are, now, of academic interest only. (shrug)
Kent Paul Dolan
> What exactly is wrong with possibility of some
> people having an ability to communicate with those
> we consider dead?
Mostly because every time a claim for someone being
able to communicate with the dead has been
examined by an investigator skilled at detecting
fraud, fraud has been found.
Harry Houdini famously exposed claims of mediums to
Seanpit wrote:
> "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>> Um, humans and chimps are 98.5% identical in
>> their DNA.
> Depends on what part of the genome you're looking
> at. This 98.5% number is usually based on
> homologies of protein-coding genes. However,
> non-coding functional DNA elements, like miRNA
> producing regions of the genome, can be much more
> different. For example, miRNAs from the brains of
> humans and chimps show an overlap of only 83%.
Oh, now _there's_ some voodoo math: if we look at
the whole genome, the fraction of differences is
small, but if we look at the part of that genome
where _most of the changes are concentrated_, the
fraction of differences is larger.
Do you even bother to insert your brain any more
when you get out of bed?
If so, why? You _never_ use it.
Oh, and I just found your online photo. You really
do display that look of mad fanaticism so visible in
the face of Kent Hovind.
xanthian.
Kent Paul Dolan
> I've explained it to you several times now.
> Humans and apes cannot produce viable much less
> fertile offspring while all of the examples you've
> listed so far can produce viable offspring.
I'd really be interested in _verifiable_ claims that
this cross has ever even been tried.
No undocumented rumors about Dr. Josef Mengele's
_really_ secret research need apply.
A female chimp trying to carry a part-human baby to
term would presumably die in childbirth due to the
expected disparity of size of the fetus head
compared to the size of the chimp mother's birth
canal.
A part-chimp fetus in a human mother is unlikely
simply because getting consent from the prospective
mother would be roughly impossible, and if
impregnated by force, she'd be likely to suicide.
Also, since human mothers already have problems
carrying some _human_ fetus's to term, she'd likely
die of something akin to blood type incompatibility,
or she'd terminate the fetus ditto.
Even an in-vitro attempt to create a fertile cross
species egg either way would have great difficulty
receiving approval from a medical research ethics
review panel today.
There are enough perfectly ordinary humans who look
much like chimps to fuel such rumors (I saw one on
the bus yesterday, dwarf short, bandy-legged, and
chimp ugly, swinging freely by his arms from the bus
passenger grab rails).
Pretending such crosses have been attempted doesn't
do much for science, proving such crosses have been
attempted under rigorous lab conditions is going to
have to be just another "Pitman Extraordinary Claim
Requiring Extraordinary Proof".
Contrariwise, arguing that such crosses are
impossible simply because they haven't been tried,
or simply because your misguided religious
prejudices insist that humans and chimps are
"different kinds" and therefore cannot be
interfertile _by religious proclamation_, is also an
Extraordinary Claim that you are nowhere close to
proving.
xanthian.
Sapient Fridge
<ac07a347-d82d-4c41...@l33g2000pri.googlegroups.com>,
seanpi...@naturalselection.0catch.com writes
>New genetic information can appear via random mechanisms. It happens
>all the time very rapidly and very commonly. It just doesn't happen
>beyond very low levels of functional complexity. There is an
>observable limit to evolutionary progress via the mechanism of RM/NS.
>There is also an observable stalling out effect that is exponential in
>nature. That's the problem.
You state this "exponential" stalling as if it were a fact, but you
never answer any post which asks for the data which shows it. I'll ask
for your data again, even though I know you either not answer or will
reply with hand-waving, evasion, unsupported assertions and probably a
pointer to a completely irrelevant study on another subject.
The one thing you won't do is provide the data.
We know there are many proteins both below and above your 1000aa
"barrier", therefore for you to be able to assert that there is an
exponential stalling out of evolved proteins you *must* be able to tell
the difference between evolved and designed proteins. You can't make
your assertion otherwise.
If you have this data then it should yield two graphs, one for designed
proteins and one for evolved proteins. The X axis of each graph being
protein length and the Y axis being frequency of proteins of that
length.
Remember that when the data from the two graphs is added together then
the resulting combined graph should look like this:
http://mbe.oxfordjournals.org/content/vol20/issue12/images/large/mbev-20-11-14-f02.jpeg
If you have this data then show us your graphs. If you don't have the
data then you have *no* basis for claiming that there is an observed
exponential drop-off in the length of evolved proteins.
--
sapient_...@spamsights.org ICQ #17887309 * Save the net *
Grok: http://spam.abuse.net http://www.cauce.org * nuke a spammer *
Find: http://www.samspade.org http://www.netdemon.net * today *
Kill: http://spamsights.org http://spews.org http://spamhaus.org
hersheyh
Of course, as any evolutionary biologist would point out, the relevant
"sequence space" for generating both modern chimps and modern humans
starts with the likely sequence of their common ancestor rather than
with "total sequence space" covering all possible genomes the size of
the human and/or chimp and/or ancestor genome. Caculating the
probability of some human gene sequence by dividing by 'total sequence
space" as if that sequence had to emerge from scratch is, well, just
plain ignorant GIGO numerology.
This ancestral "sequence space" is going to be about 98% identical to
the sequence in *both* humans and chimp. That is, it is going to need
to change only marginally. And we *know* that RM/NS (in fact, RM and
neutral drift for most of it) occurs at a sufficient rate to account
for the observed differences.
If Sean knows of any place or requirement in the genome where he
thinks RM/NS *cannot* have produced the observed difference, he is
welcome to present it. Until he does, he has nothing but wishful
thinking.
unrestra...@hotmail.com
> On 1 Dec, 18:00, hersheyh <hershe...@yahoo.com> wrote:
>
>
>
> > On Dec 1, 6:21 pm, Seanpit <seanpitnos...@naturalselection.0catch.com>> > [snip]
>
> > > That's right. The odds of finding a novel beneficial 300aa target are
> > > exponentially greater than the odds of finding a novel 1000aa target
> > > because the ratio of targets vs. non-targets is exponentially greater
> > > at the 300aa level vs. the 1000aa level.
>
> > You say "exponentially greater". How much greater is that? Let's use
> > 333aa and 1000aa systems. The 1000aa system is linearly 3 times
> > larger than the 333aa system. How many times larger is the
> > "exponential" difficulty of finding a beneficial target in the 1000aa
> > system than in the 333aa system that is 1/3 the size? Nine? Twenty-
> > seven? Tell me what *you* mean by "exponentially greater"?
>
> There is a linear increase in the likely gap distance between anything
> in a particular genome and the likely distance to the closest
> potentially beneficial sequence (i.e., target) at a particular degree
> of minimum specificity with increasing sequence size requirements.
> Each linear increase in the gap distance translates into an
> exponential increase in the number of random mutations needed to cross
> the gap by 20 fold. So, if the gap distance increased from 1 to 50 as
> the threshold increased from 333 fsaar to 1000, the number of
> mutations needed to cross the gap would increase by 20^N - - or 20^50
> in this case.
>
> For further detail see:
>
> http://www.detectingdesign.com/flagellum.html#Calculation
>
> Sean Pitmanwww.DetectingDesign.com
What's to stop a a 300aa gene from duplicating, then duplicating a
section of that - two mutations perhaps, probably neutral - then one
additional mutation, say, a reversal of one section of 50 aa on the
string? Four mutations leading to an additional 700aa, witha
profoundly different order. Not so many mutations to get there.
And you still haven't explained how you know how many of these
possible mutations are beneficial. Remember, evolutionary theory does
not describe a teleological process.
So, four mutations to get to a hypothetical target, our of an unknown
proportion of beneficial targets. What's the big deal?
Kermit
Kermit
unrestra...@hotmail.com
> On 1 Dec, 20:11, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
>
>
> > On Dec 1, 10:55 pm, Seanpit <sean...@gmail.com> wrote:
>
> > > Yes, it is. There are a great many potential targets or "winning
> > > numbers" within the lottery of sequence space at each level of
> > > functional complexity - trillions upon trillions of them even for 100
> > > fsaar systems. The problem, of course, is that there are a great many
> > > more non-beneficial sequences. The odds of ending up upon any one of
> > > them involved probability analyzes.
>
> > That's nice.
>
> > Why,. again, is the "probability" of a jaguar evolving from another
> > cat (a cheetah, say) greater than the "probability" of a human
> > evolving from a (much mnore closely genetically-related) chimp?
>
> Mendelian variation isn't the evolution of anything new, functionally
> new, within the genome of a qualitative nature. Big cat variations
> are not based on anything other than Mendelian variation - not real
> evolution of novel genetic functional features within the genome.
>
> This could also be true of humans and apes, but is less likely due to
> the fact that humans and apes cannot produce viable much less fertile
> hybrid offspring. There are also likely functional brain differences
> as well,
Excuse me? "Likely" functional brain differences? What are teh odds?
Can yu even describe these brain differences at the cellular level? I
thought you said it wasn't science unles syou can do the math.
At least we can show the genomes (of the organisms we have analyzed),
but you keep saying that unless we can show the math, the actual
evidence doesn't mean anything.
Well, show the math for these likely but unspecified differences.
>down to the cellular level, which are likely based on
> significant differences in functional non-coding DNA sequences.
>
> > Show me your math, Sean.
>
> > ================================================
> > Lenny Flank
> > "There are no loose threads in the web of life"
>
> > Editor, Red and Black Publishershttp://www.RedandBlackPublishers.com
>
> Sean Pitmanwww.DetectingDesign.com
Kermit
gregwrld
As I understand it he's claiming
these changes can't produce
"novel" functions - whatever he
means by "novel".
gregwrld
wf3h
>
> So, four mutations to get to a hypothetical target, our of an unknown
> proportion of beneficial targets. What's the big deal?
>
you're leaving out god. and that will never do
hersheyh
> On Dec 1, 8:25 pm, Seanpit <sean...@gmail.com> wrote:
>
>
>
> > On 1 Dec, 20:11, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
> > > On Dec 1, 10:55 pm, Seanpit <sean...@gmail.com> wrote:
>
> > > > Yes, it is. There are a great many potential targets or "winning
> > > > numbers" within the lottery of sequence space at each level of
> > > > functional complexity - trillions upon trillions of them even for 100
> > > > fsaar systems. The problem, of course, is that there are a great many
> > > > more non-beneficial sequences. The odds of ending up upon any one of
> > > > them involved probability analyzes.
>
> > > That's nice.
>
> > > Why,. again, is the "probability" of a jaguar evolving from another
> > > cat (a cheetah, say) greater than the "probability" of a human
> > > evolving from a (much mnore closely genetically-related) chimp?
>
> > Mendelian variation isn't the evolution of anything new, functionally
> > new, within the genome of a qualitative nature. Big cat variations
> > are not based on anything other than Mendelian variation - not real
> > evolution of novel genetic functional features within the genome.
>
> > This could also be true of humans and apes, but is less likely due to
> > the fact that humans and apes cannot produce viable much less fertile
> > hybrid offspring. There are also likely functional brain differences
> > as well,
>
> Excuse me? "Likely" functional brain differences?
Remember that what he needs is a *large* qualitative difference that
requires crossing a *large* functionless gap. Hill-climbing
quantitative differences in brain function will simply not do. He
already knows that the last person to claim a significant
*qualitative* difference in the ape and human brain was Richard Owen.
He "found" a part of the brain that humans have and apes lack: the
hippocampus minor.
http://www.ucmp.berkeley.edu/history/owen.html
So now what he is doing is weaving a not-just-so tale about some
magical event involving changes in a bunch of miRNA sequence changes
having to magically poof into existence all at once (rather than
serially, as would be expected) to produce some as yet unspecified
"difference" between humans and other apes. He proposes this
hypothetical and untestable (at least until he tells us of some actual
qualitative phenotypic difference between apes and humans) idea as a
last ditch try to avoid facing the fact that the amount of difference
between humans and apes is perfectly consistent with RM and neutral
drift or, in some cases, the faster NS.
'Rev Dr' Lenny Flank
> On 1 Dec, 20:11, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
>
>
>
>
> > On Dec 1, 10:55 pm, Seanpit <sean...@gmail.com> wrote:
>
> > > Yes, it is. There are a great many potential targets or "winning
> > > numbers" within the lottery of sequence space at each level of
> > > functional complexity - trillions upon trillions of them even for 100
> > > fsaar systems. The problem, of course, is that there are a great many
> > > more non-beneficial sequences. The odds of ending up upon any one of
> > > them involved probability analyzes.
>
> > That's nice.
>
> > Why,. again, is the "probability" of a jaguar evolving from another
> > cat (a cheetah, say) greater than the "probability" of a human
> > evolving from a (much mnore closely genetically-related) chimp?
>
> Mendelian variation isn't the evolution of anything new, functionally
> new, within the genome of a qualitative nature. Big cat variations
> are not based on anything other than Mendelian variation - not real
> evolution of novel genetic functional features within the genome.
>
> This could also be true of humans and apes, but is less likely due to
> the fact that humans and apes cannot produce viable much less fertile
> hybrid offspring. There are also likely functional brain differences
> significant differences in functional non-coding DNA sequences.
That's nice. (yawn)
But I, uh, don't see any math here, Sean . . . . . .
Did you forget that part?
Here, let me walk you through it step by step, Sean:
1. What is the "probability" of a jaguar evolving from a cheetah, and
how do you calculate that "probability"?
2. What is the "probability" of a human evolving from a chimp, and
how do you calculate THAT "probability"?
3. Which probability is higher?
I don't want to see any of your "it looks that way to ME" baloney,
Sean.
Just show me your math.
Unless, of course, you don't HAVE any . . . . . . . . . . ?
'Rev Dr' Lenny Flank
(snip). He proposes this
> hypothetical and untestable (at least until he tells us of some actual
> qualitative phenotypic difference between apes and humans) idea as a
> last ditch try to avoid facing the fact that the amount of difference
> between humans and apes is perfectly consistent with RM and neutral
> drift or, in some cases, the faster NS.
>
And indeed, as he well knows, humans and chimps are much closer,
genetically, than many of the specvies that even he accept evolved
from each other.
I won't even ASK him to explain why humans have a chromosome that
looks, uh, exactly like two fused chimp
chromosomes . . . . . . . . . . . . .
'Rev Dr' Lenny Flank
> On Dec 4, 12:24 pm, seanpitnos...@naturalselection.0catch.com wrote:
>
> >There is an
> > observable limit to evolutionary progress via the mechanism of RM/NS.
>
> Really. . . .
>
> What.
>
> What is this "limit", how is it produced, and what mechanism is it
> that allows genetic changes to happen within this "limit" but prevents
> any genetic changes from crossing this "limit"?
Hey Sean, you seem to have forgotten to answer this simple quesdtion.
So I'm asking again.
And I'll ask again. And again. And again and again and again, as
many times as I need to till I get an answer.
I'm a very patient man.
Seanpit
wrote:
That's exactly my point. This is why the popular concept of "species"
is so subjective.
> Now if there are large quantitative genetic differences between
> populations, one has a reason to expect that there might be a reason for
> those differences, presumably a lack of significant gene flow, and
> depending on your species concept you might suppose they are different
> species. But genetic difference isn't the criterion, merely a clue.
>
> One of which you should get.
I understand the popular definition of "species" just fine. I just
don't think it means much. It is far too subjective to be very
useful.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Dec 3, 1:27 am, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
>
>
> > On Dec 2, 10:04 pm, Seanpit <sean...@gmail.com> wrote:
>
> > Such differences are largely the
>
> > > result of Mendelian-type variation within an otherwise static gene
> > > pool of options.
>
> > Would a descendent species that has a single chromosome produced by
> > the fusion of two different chromosomes in its ancestor, count, in
> > your view, as a "Mendelian-type variation within an otherwise static
> > gene pool of options"?
This isn't exactly "Mendelian", but it could still be part of the same
gene pool as long as there is no qualitative difference in function
produced - i.e., just a quantitative or neutral difference in
function.
> > Even if it meant that the two species could no longer produce viable
> > zygotes?
Producing viable zygotes is irrelevant to my view of the same "kind"
of gene pool - i.e., a functional definition of a gene pool.
> > Why nor why not?
>
> A related question:
>
> If the descendent species had a large inversion of gene sequence in a
> critical area of its chromosome, as compared to its ancestor, which
> prevented them from forming a viable zygote, would that too count, in
> your view, as a "Mendelian-type variation within an otherwise static
> gene pool of options"?
Again, this isn't exactly a Mendelian-type variation, but it is a
variation within the same static gene pool of functional options -
qualitatively speaking.
> Why nor why not?
>
> And perhaps you could expand upon your answer by citing an example of
> the sort of hypothetical genetic change that you would consider to NOT
> be a "Mendelian-type variation within an otherwise static gene pool of
> options"?
Any mutation that produces a qualitatively novel functional system
that was not in the gene pool of options before would count as going
beyond the "static" options of the gene pool. For example, the
evolution of various single protein enzymes, like lactase, nylonase,
citrase, etc., would all count.
> And don't forget, I am still waiting to hear how we can measure "gaps
> in sequence space", how we can tell whether the gap between species A
> and B is larger than or smaller than the gap between species C and D,
> and how you can calculate the, um, "statistical probability" of either
> of these gaps being crossed when you, uh, don't know how big they are
> or how to measure them. . . .
You calculate gap distances based on the minimum number of mutations
needed to produce a qualitatively novel functional difference between
"A" and "B".
> (And I'd prefer it greatly if you'd answer these simple questions,
> rather than avoiding them and thereby making me ask them again and
> again and again and again until you either answer or run away, like
> most creationists do.)
I've already answered these questions before for you; some of them
many times already.
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
'Rev Dr' Lenny Flank
Can you give us a non-subjective, useful, definition of a "kind", a
"novel function", and a "gap in sequence space"?
Oh, and you mentioned something about a "limit" to genetic change --
can you tell us what that limit results from, and what mechanism you
think acts to allow genetic changes within this limit but prevents any
genetic changes from occuring outside this lkimit?
Thanks in advance for not answering.
I'll ask again later.
John Harshman
You frequently say that your point is completely the opposite of what
you said your point was originally. I take that as a sign that you
either are a very poor writer, and didn't originally say what you meant,
or a very poor reader, and don't understand what I just said. Whichever
it is, there's no way for me to proceed.
>> Now if there are large quantitative genetic differences between
>> populations, one has a reason to expect that there might be a reason for
>> those differences, presumably a lack of significant gene flow, and
>> depending on your species concept you might suppose they are different
>> species. But genetic difference isn't the criterion, merely a clue.
>>
>> One of which you should get.
>
> I understand the popular definition of "species" just fine. I just
> don't think it means much. It is far too subjective to be very
> useful.
Hard to tell, since I have no idea what you understand the popular
definition of "species" to be. You had originally claimed that species
were often defined by quantitative genetic differences. I told you this
is wrong, that species are never defined that way. And you said that was
your point. Can you understand my confusion?
Seanpit
wrote:
< snip >
> >> What makes the most sense is counting mutations. Humans and chimps
> >> differ by 40 million mutations. 35 million of those are point
> >> substitutions. 5 million are indels. There are a negligible few more
> >> that don't fall into either category, such as chromosomal fusions,
> >> inversions, and perhaps a few more categories I'm not thinking of.
>
> > Yeah - and modern humans can have this many individual mutational
> > differences with the next-door neighbor when it comes to absolute
> > numbers when one isn't concerned about the quality of the difference
> > (i.e., size and/or functional features).
>
> What do you mean by "this many"? Are you claiming that next-door
> neighbors can differ by as many as 40 million mutations? Show me some
> evidence for that claim, if so.
Is a duplication, or loss, of a region of DNA, in one person relative
to another, a "mutation" in your book?
< snip rest for now >
Sean Pitman
www.DetectingDesign.com
Seanpit
Also, consider that the Human Genome Project suggests a higher
concentration of SNPs than previously thought. Current estimates
suggest that "SNPs . . . occur every 100 to 300 bases along the 3-
billion-base human genome."
http://www.ornl.gov/sci/techresources/Human_Genome/faq/snps.shtml
Of course, that implies that an individual will have upwards of 30
million SNPs alone.
And, SNPs are common within other species as well - like maize and
cattle, both of which average 1 SNP per 100 bp of DNA. (approximately
30 million sites in cattle) .... "1 SNP occurs every 100 bp when
comparing the 96 diverse beef sires from 19 breeds."
That's within a single "species" of cattle - which is similar to your
proposed difference between humans and chimps and at least part of the
basis for your claim for different species classification.
Obviously, such mutational differences don't necessarily correlate
with species classifications. It seems like numbers alone, without
any consideration of functional quality, don't mean much. Again,
functional quality trumps quantity. And, this isn't even considering
the latest information on CNV mutations . . .
"The extent of the variation was breathtaking: these relatively
common CNVs cumulatively affected 360 million nucleotides, or about
12% of the human genome: one of a homologous pair of chromosomes could
be a million nucleotides and 20 genes shorter than the other. The
comforting idea arising from the SNP map that any 2 humans were more
than 99.7% identical at the genomic level was suddenly shattered."
http://www.stanford.edu/class/cs273a/papers.aut07/lecture5/cnvOpinion.pdf
Sean Pitman
www.DetectingDesign.com
Seanpit
wrote:
The point is that there are all kinds of definitions for the term
"species". It all depends on what you want it to mean. There is no
clear consensus on what it really means to be a separate "species"
that is consistently reproducible.
"A species is often defined as a group of organisms capable of
interbreeding and producing fertile offspring. While in many cases
this definition is adequate, more precise or differing measures are
often used, such as based on similarity of DNA or morphology. Presence
of specific locally adapted traits may further subdivide species into
subspecies."
http://en.wikipedia.org/wiki/Species
So, here we have a definition based on producing fertile offspring or
DNA or morphologic similarity. Yet, according to you, the production
of fertile offspring can be done between "species" - as long as it
isn't too common. You also argue that a species need not have any
genetically isolating mechanism at all - as long as there is some sort
of geographical or time separation where there is no gene flow - even
though there could easily be or have been gene flow without this
physical separation of time and/or place.
And you call such definitions scientifically meaningful? This is
complete nonsense as far as I can tell. Just because a group of dogs
gets isolated and doesn't breed with other dogs for a while doesn't by
itself make them anything other than dogs. I mean really, by this
definition certain groups of long-isolated humans, like aborigines,
would be classified as a different non-human species. That's
ridiculous.
> >> Now if there are large quantitative genetic differences between
> >> populations, one has a reason to expect that there might be a reason for
> >> those differences, presumably a lack of significant gene flow, and
> >> depending on your species concept you might suppose they are different
> >> species. But genetic difference isn't the criterion, merely a clue.
>
> >> One of which you should get.
>
> > I understand the popular definition of "species" just fine. I just
> > don't think it means much. It is far too subjective to be very
> > useful.
>
> Hard to tell, since I have no idea what you understand the popular
> definition of "species" to be.
Nobody does. That's the problem with the term. It is too subjective.
> You had originally claimed that species
> were often defined by quantitative genetic differences.
They can be.
> I told you this
> is wrong, that species are never defined that way.
And you were/are mistaken. Species are often defined by nothing more
than quantitative differences. That is why, on occasion, different
sexes within the same breeding group have been given different species
names - or even different parts of the same plant. This is also why
different morphologies that are based only on quantitative differences
in genetic expression are also given different species names on
occasion. Sure, they may also have happened to have been isolated for
a while in time or place, but this is no reason, by itself, to
separate groups into different species classifications.
> And you said that was
> your point. Can you understand my confusion?
Not any more than a general confusion over the concept of
"species" . . .
Sean Pitman
www.DetectingDesign.com
Ron O
It is a single mutation if tandem and a double mutation if there has
been a duplication and insertion translocation to somewhere else in
the genome. Most translocations are single mutational events. The
same for inversions. Only someone that couldn't count and didn't know
what they were talking about would count all the base-pairs in a
duplication as individual mutations. I work with a duplication of
180,000 base-pairs of the Z sex chromosome and If I claimed that I was
working with 180,000 mutations instead of a single tandem duplication
event in a publication what do you think would happen?
'Rev Dr' Lenny Flank
>
> The point is that there are all kinds of definitions for the term
> "species". It all depends on what you want it to mean. There is no
> clear consensus on what it really means to be a separate "species"
> that is consistently reproducible.
>
How about a "kind", Sean. Can you give us a consistently reproducible
definition of that? One that doesn't jsut depend on what you want it
to mean?
By the way, how, again, do we measure the "gasp in sequence space"
between any two species? How, again, do we know if one "gap" is
bigger and less "probable" than another? How again do we calculate
that? Show me your math, Sean.
(sound of crickets chirping)
You have nothing to offer, Sean. Nothing.
Ron O
This has been about the estimate since before they had the genome
sequence and it isn't for individuals, but the estimate is for groups
of individuals. If you got around 30 people together as a group they
would differ from at least one other member of the group every 300
base-pairs. Any two individuals of the group might vary by around one
SNP every 1000 base-pairs. Any individual of the group might vary by
a SNP every 50 to 100 base-pairs from a chimp. If we took around 500
million to a billion people we would likely find a SNP at just about
every position of the genome just due to new mutations inherited from
their parents.
This doesn't help any of your arguments. What would help it is if the
variation was much less. We know that humans do not have as much
genetic variation as most other species. Other species usually have 5
times the variation found in humans. If you took a diverse group of
30 domestic chickens you would find a SNP every 30 base-pairs. Hey
Sean, you might differ from a chimp by a SNP every 50 base-pairs. The
normal population is full of genetic variation. This is what makes
rapid natural selection possible. Studies like the Golapagos finch
study shows us that populations can change over 4 orders of magnitude
faster than the average seen in the fossil record over short periods
of time.
>
> And, SNPs are common within other species as well - like maize and
> cattle, both of which average 1 SNP per 100 bp of DNA. (approximately
> 30 million sites in cattle) .... "1 SNP occurs every 100 bp when
> comparing the 96 diverse beef sires from 19 breeds."
See, they needed 96 sires and got a whole lot of genetic variation.
So what is your beef. You can't just blow smoke about these issues
and expect everyone to forget that the data just makes your
alternative less likely. Cattle aren't much better off than humans.
A better example would be chickens, but it still wouldn't be a better
example for you would it? You can't explain the genetic variation in
humans so why should you be able to explain the genetic variation in
chickens.
How long does it take to generate this amount of genetic diversity?
Humans share genetic diversity with chimps. That means that some of
the genetic diversity in our human population is probably over 5
million years old. We know where it is coming from. Most of it comes
from our ancestors. We can even estimate that we went through at
least 1 major bottleneck in our population and lost most of our
genetic variation during that event. You can take a population with
low genetic diversity like cheetahs and watch them over time to see
how much diversity is generated. If you monitor things like
population size and generation length you can see if it matches what
is predicted by population genetic theory. What can you do?
>
> That's within a single "species" of cattle - which is similar to your
> proposed difference between humans and chimps and at least part of the
> basis for your claim for different species classification.
> Obviously, such mutational differences don't necessarily correlate
> with species classifications. It seems like numbers alone, without
> any consideration of functional quality, don't mean much. Again,
> functional quality trumps quantity. And, this isn't even considering
> the latest information on CNV mutations . . .
What is your explanation for the data? What a joker. We can look at
extant populations and figure out species diversity and its
association with biological evolution, but what is your explanation
for all this genetic diversity? You can't just blow smoke. You have
to explain this junk too. We have an explanation that works. Do you
deny population genetics works? How are you going to explain how we
have been able to create the green revolution? How was the neutral
theory for a lot of genetic variation vindicated? How do you explain
the "neutral" variation? I can tell you that breeding companies use
very sophisticated breeding value estimation programs to select their
breeders. What do you have? How can you verify it? We have graphs
showing that it used to take 15 weeks to grow a chicken to 3.5 lbs in
the 1950s, but we can grow a chicken to 5 lbs in 6 weeks and have
decrease the mortality from 15% to around 4%. Feed efficiency has
gone from around 3 kg of feed for every kg of carcass to around 1.8 kg
feed for every kg of carcass. If we calculate to 3.5 lb carcass the
feed efficiency is better because you have less to support with later
growth and the efficiency is around 1.4. So it used to take around
10.5 lbs of feed to grow a 1950s chicken, and with selection we can
make that weight with half the feed in less than 1/3 the time.
Contrary to popular belief the chicken industry does not use hormones
like the beef industry, and we do not put antibiotics in the feed we
feed our chickens.
You just have to look at a toy pug and compare it to an Irish wolf
hound to see what selection can do. What do you have?
>
> "The extent of the variation was breathtaking: these relatively
> common CNVs cumulatively affected 360 million nucleotides, or about
> 12% of the human genome: one of a homologous pair of chromosomes could
> be a million nucleotides and 20 genes shorter than the other. The
> comforting idea arising from the SNP map that any 2 humans were more
> than 99.7% identical at the genomic level was suddenly shattered."
>
> http://www.stanford.edu/class/cs273a/papers.aut07/lecture5/cnvOpinion...
All things that you can't deal with. Does everyone know what CNVs
are? They are copy number variants. With the new molecular
technologies developed within the last 10 years we have been able to
study CNVs. This is one of the types of mutations that we have
thought is one of the prime necessities for generating new proteins
that do different things. Sean should be crying about the fact that
we find that CNVs are very common. He just has to go to his 1000 aa
bull pucky of the flagellum example and look to see how many of the
proteins are due to past CNV events to know that he is sunk, but he
keeps blowing smoke anyways. It is so bogus to use CNVs as a smoke
screen when you have to know that Sean wishes that they didn't even
exist.
Where is that alternative to common descent and the evidence to back
it up that is just as good as what real science has? Where is that
science of intelligent design that you would have taught to school
kids? You can run and pretend and try dishonest deflection ploys, but
that doesn't produce what you need. No scientific alternative, no
science worth teaching, no honest argument. Now, if you started to
argue theology you probably could engage in an honest argument if you
could control your dishonest behavior, but trying to argue the science
with what you know is just bogus.
>
> Sean Pitmanwww.DetectingDesign.com-
Still lying in the title of your web page.
Where is that science of intelligent design that you would have taught
to school kids? Why doesn't your 1000 aa bull pucky make the grade?
If you know why it doesn't make the grade why put it forward until it
does make the grade, or at least tell people up front that it isn't
worth jack compared to what you are arguing against? Why lie to
people about this junk?
Ron Okimoto
John Harshman
Of course it is. One mutation. Now can you answer the question?
hersheyh
[snip]
>
> Any mutation that produces a qualitatively novel functional system
> that was not in the gene pool of options before would count as going
> beyond the "static" options of the gene pool. For example, the
> evolution of various single protein enzymes, like lactase, nylonase,
> citrase, etc., would all count.
And what theory of evolution proposes that novel functional systems
arise from something that "was not in the gene pool of options", that
involves creating something "beyond the "static" options of the gene
pool"?
In fact, even for the single protein enzymes you describe, they do not
arise in some organisms and do arise in others. The ones they arise
in include, in the "'static' options of [their specific] gene pool"
*specific* sequences that can be modified within their "gene pool of
options" to produce that new function. The organisms in which the
feature fails to arise, lack those options.
What does that mechanism of "descent with modification" have to do
with your 'evolutionary' mechanism involving starting from some random
site in total sequence space, when no organism has either "total
sequence space" nor do organisms have random samples of total sequence
space in their real sequence space?
But, yes, if you are positing a starting point that must be "outside"
the "gene pool of options" that could lead to a novel system, then
that novel system cannot arise. But that is some sort of logical
error...assuming your conclusion, I believe. I could do the same
thing with the smaller proteins. If I assume a starting point of an
organism that has no sequence that can be easily modified to lactase
function, then lactase function will definitely be much harder to
evolve. As Homer would say, "Doh!"
[snip]
John Harshman
No it doesn't, not in the sense you mean. It means that every individual
will have 30 million SNP sites, but nobody will have 30 million of the
rare alleles. No two individuals will be separated by 30 million SNPs.
> And, SNPs are common within other species as well - like maize and
> cattle, both of which average 1 SNP per 100 bp of DNA. (approximately
> 30 million sites in cattle) .... "1 SNP occurs every 100 bp when
> comparing the 96 diverse beef sires from 19 breeds."
>
> That's within a single "species" of cattle - which is similar to your
> proposed difference between humans and chimps and at least part of the
> basis for your claim for different species classification.
No. It's not at all part of that basis, as I keep telling you. And
please don't confuse the extent of polymorphism spread over an entire
population with the genetic distance between individuals.
> Obviously, such mutational differences don't necessarily correlate
> with species classifications. It seems like numbers alone, without
> any consideration of functional quality, don't mean much. Again,
> functional quality trumps quantity. And, this isn't even considering
> the latest information on CNV mutations . . .
You seem not even to be reading anything I say.
> "The extent of the variation was breathtaking: these relatively
> common CNVs cumulatively affected 360 million nucleotides, or about
> 12% of the human genome: one of a homologous pair of chromosomes could
> be a million nucleotides and 20 genes shorter than the other. The
> comforting idea arising from the SNP map that any 2 humans were more
> than 99.7% identical at the genomic level was suddenly shattered."
>
> http://www.stanford.edu/class/cs273a/papers.aut07/lecture5/cnvOpinion.pdf
Have you factored in the CNV differences between a given human and a
given chimp?
John Harshman
Hey, that's the third "the point" so far.
> "A species is often defined as a group of organisms capable of
> interbreeding and producing fertile offspring. While in many cases
> this definition is adequate, more precise or differing measures are
> often used, such as based on similarity of DNA or morphology. Presence
> of specific locally adapted traits may further subdivide species into
> subspecies."
>
> http://en.wikipedia.org/wiki/Species
>
> So, here we have a definition based on producing fertile offspring or
> DNA or morphologic similarity. Yet, according to you, the production
> of fertile offspring can be done between "species" - as long as it
> isn't too common. You also argue that a species need not have any
> genetically isolating mechanism at all - as long as there is some sort
> of geographical or time separation where there is no gene flow - even
> though there could easily be or have been gene flow without this
> physical separation of time and/or place.
Wikipedia is in this case just wrong about what "species" means to a
biologist. Do you imagine that I, a practicing biologist, am more likely
to be mistaken about the concept of "species" than something you
happened to pull off the web?
> And you call such definitions scientifically meaningful? This is
> complete nonsense as far as I can tell. Just because a group of dogs
> gets isolated and doesn't breed with other dogs for a while doesn't by
> itself make them anything other than dogs. I mean really, by this
> definition certain groups of long-isolated humans, like aborigines,
> would be classified as a different non-human species. That's
> ridiculous.
Agreed that it would be ridiculous. But you completely misunderstand the
species concepts you criticize. Your ignorance of biology is causing the
usual problems.
>>>> Now if there are large quantitative genetic differences between
>>>> populations, one has a reason to expect that there might be a reason for
>>>> those differences, presumably a lack of significant gene flow, and
>>>> depending on your species concept you might suppose they are different
>>>> species. But genetic difference isn't the criterion, merely a clue.
>>>> One of which you should get.
>>> I understand the popular definition of "species" just fine. I just
>>> don't think it means much. It is far too subjective to be very
>>> useful.
>> Hard to tell, since I have no idea what you understand the popular
>> definition of "species" to be.
>
> Nobody does. That's the problem with the term. It is too subjective.
I disagree. Now of course species are fuzzy entities in many cases,
because speciation is a gradual process. Given branching evolution,
there will be intermediate conditions between 1 species and 2 species in
many cases. But those cases are a fairly small proportion. Most often,
different species concepts agree in practice, given enough data to make
a judgment.
>> You had originally claimed that species
>> were often defined by quantitative genetic differences.
>
> They can be.
I suppose anything can, hypothetically, be defined by anything, since
anyone can make a definition. But species have never been so defined in
my experience.
>> I told you this
>> is wrong, that species are never defined that way.
>
> And you were/are mistaken. Species are often defined by nothing more
> than quantitative differences. That is why, on occasion, different
> sexes within the same breeding group have been given different species
> names - or even different parts of the same plant. This is also why
> different morphologies that are based only on quantitative differences
> in genetic expression are also given different species names on
> occasion. Sure, they may also have happened to have been isolated for
> a while in time or place, but this is no reason, by itself, to
> separate groups into different species classifications.
Here is the nub of some of your confusion. You mistake definition with
diagnosis. You didn't pay attention when I said this the first time, but
maybe second time is the charm? Genetic and morphological differences
are used as clues to species status, not as definitions. That's why when
different sexes are described as different species (and I know of only
one real example, Eclectus), that designation is removed when the truth
becomes known.
Really, now. How would you feel if I tried to lecture you on the proper
way to remove a gall bladder? You know very little about species and
species concepts, despite your ability to google voluminous quotes on
the subject.
>> And you said that was
>> your point. Can you understand my confusion?
>
> Not any more than a general confusion over the concept of
> "species" . . .
I am beginning to suspect that you are both a very bad writer and a very
bad reader.
John S. Wilkins
> Seanpit wrote:
...
> > "A species is often defined as a group of organisms capable of
> > interbreeding and producing fertile offspring. While in many cases
> > this definition is adequate, more precise or differing measures are
> > often used, such as based on similarity of DNA or morphology. Presence
> > of specific locally adapted traits may further subdivide species into
> > subspecies."
> >
> > http://en.wikipedia.org/wiki/Species
> >
> > So, here we have a definition based on producing fertile offspring or
> > DNA or morphologic similarity. Yet, according to you, the production
> > of fertile offspring can be done between "species" - as long as it
> > isn't too common. You also argue that a species need not have any
> > genetically isolating mechanism at all - as long as there is some sort
> > of geographical or time separation where there is no gene flow - even
> > though there could easily be or have been gene flow without this
> > physical separation of time and/or place.
>
> Wikipedia is in this case just wrong about what "species" means to a
> biologist. Do you imagine that I, a practicing biologist, am more likely
> to be mistaken about the concept of "species" than something you
> happened to pull off the web?
It has become clear to me that "species" is a term that has different
significations to different disciplines. A large part of the "species
problem" is down to this. Molecular biologists often do hold the
definition Wikipedia quotes. It is, of course, putting the diagnostic
cart before the causal horse...
This in no way supports Sean; just sayin'...
...
--
John S. Wilkins, Philosophy, University of Sydney
scienceblogs.com/evolvingthoughts
But al be that he was a philosophre,
Yet hadde he but litel gold in cofre
John Harshman
a tiny bit of truth. Some of the wilder proponents of DNA barcoding have
claimed that you can use the barcode to reliably define new species. But
that's a fringe view.
John S. Wilkins
Not a fringe view - it is becoming increasingly widespread. For example,
T. Ryan Gregory has been promoting it, and attacks anyone who criticises
it, on his blog. I made the mistake of attacking it earlier this year,
and he came at me with all kinds of rhetorical flourishes of the kind we
normally associate with ID.
Moreover, barcoding is getting government funding (which pisses me off
no end as it seems to be largely driven by a single company) as a
replacement for field taxonomy and ecology. It's a technosolution to a
problem that is multivariate and costly, so of course bureaucrats love
it.
There are definitions of "species" that rely on molecular clustering
(e.g., Jim Mallet's, and possibly Templeton's suitably interpreted)
although some earlier ones (e.g., Cracraft's and Eldredge's) had talked
about diagnosable clusters of individuals' traits.
John Harshman
How is this evidence that it's not a fringe view? Quite the opposite, it
seems to me.
> Moreover, barcoding is getting government funding (which pisses me off
> no end as it seems to be largely driven by a single company) as a
> replacement for field taxonomy and ecology. It's a technosolution to a
> problem that is multivariate and costly, so of course bureaucrats love
> it.
Let's not start trading barcoding rants.
> There are definitions of "species" that rely on molecular clustering
> (e.g., Jim Mallet's, and possibly Templeton's suitably interpreted)
> although some earlier ones (e.g., Cracraft's and Eldredge's) had talked
> about diagnosable clusters of individuals' traits.
If you actually look at what Mallet says, he also requires that these
clusters be stable in sympatry; i.e. it's a disguised form of the BSC.
'Rev Dr' Lenny Flank
> On Dec 4, 6:58 pm, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
> > On Dec 4, 12:24 pm, seanpitnos...@naturalselection.0catch.com wrote:
>
> > >There is an
> > > observable limit to evolutionary progress via the mechanism of RM/NS.
>
> > Really. . . .
>
> > What.
>
> > What is this "limit", how is it produced, and what mechanism is it
> > that allows genetic changes to happen within this "limit" but prevents
> > any genetic changes from crossing this "limit"?
>
> Hey Sean, you seem to have forgotten to answer this simple quesdtion.
>
> So I'm asking again.
>
> And I'll ask again. And again. And again and again and again, as
> many times as I need to till I get an answer.
>
> I'm a very patient man.
>
I'm still waiting, Sean . . . . . . . . .
What seems to be the problem . . . . . . ?
wf3h
>
> > > What is this "limit", how is it produced, and what mechanism is it
> > > that allows genetic changes to happen within this "limit" but prevents
> > > any genetic changes from crossing this "limit"?
>
> > Hey Sean, you seem to have forgotten to answer this simple quesdtion.
>
> > So I'm asking again.
>
> > And I'll ask again. And again. And again and again and again, as
> > many times as I need to till I get an answer.
>
> > I'm a very patient man.
>
> I'm still waiting, Sean . . . . . . . . .
>
> What seems to be the problem . . . . . . ?
you're gonna have to pull an adlai stevenson on sean, i'm afraid....if
you remember the cuban missle crisis, stevenson was US ambassador to
the UN. when the soviets refused to answer about the missiles in cuba,
stevenson said he was prepared to wait 'until hell freezes over' for
his answer
sean, i'm afraid, is playing the role of the soviet ambassador. he's
saying nothing about his 'scientific' view of creation.
seanpi...@naturalselection.0catch.com
wrote:
>
> > Also, consider that the Human Genome Project suggests a higher
> > concentration of SNPs than previously thought. Current estimates
> > suggest that "SNPs . . . occur every 100 to 300 bases along the 3-
> > billion-base human genome."
>
> >http://www.ornl.gov/sci/techresources/Human_Genome/faq/snps.shtml
>
> > Of course, that implies that an individual will have upwards of 30
> > million SNPs alone.
>
> No it doesn't, not in the sense you mean. It means that every individual
> will have 30 million SNP sites, but nobody will have 30 million of the
> rare alleles. No two individuals will be separated by 30 million SNPs.
Some estimates for the average comparison between any two people go as
high as 1 in 300 bases.
http://books.google.com/books?id=eP_kWit5278C - - Page 28
However, most person-person comparisons report averages of around 1
per 1000 bases or ~3 million SNP differences.
Yet, AFAICT, this is irrelevant as over 30 million could be sustained
without a loss of the same function and appearance needed to be
classified as a modern human - to include the ability to produce
viable and fertile offspring.
> > And, SNPs are common within other species as well - like maize and
> > cattle, both of which average 1 SNP per 100 bp of DNA. (approximately
> > 30 million sites in cattle) .... "1 SNP occurs every 100 bp when
> > comparing the 96 diverse beef sires from 19 breeds."
>
> > That's within a single "species" of cattle - which is similar to your
> > proposed difference between humans and chimps and at least part of the
> > basis for your claim for different species classification.
>
> No. It's not at all part of that basis, as I keep telling you. And
> please don't confuse the extent of polymorphism spread over an entire
> population with the genetic distance between individuals.
I don't understand your argument then. If you are not arguing that
gross numbers of mutational differences have anything to do with
species classification, what is your argument? I thought that was my
argument!
> > Obviously, such mutational differences don't necessarily correlate
> > with species classifications. It seems like numbers alone, without
> > any consideration of functional quality, don't mean much. Again,
> > functional quality trumps quantity. And, this isn't even considering
> > the latest information on CNV mutations . . .
>
> You seem not even to be reading anything I say.
I've read what you've written, but obviously I don't understand what
you're trying to say. That's quite true.
> > "The extent of the variation was breathtaking: these relatively
> > common CNVs cumulatively affected 360 million nucleotides, or about
> > 12% of the human genome: one of a homologous pair of chromosomes could
> > be a million nucleotides and 20 genes shorter than the other. The
> > comforting idea arising from the SNP map that any 2 humans were more
> > than 99.7% identical at the genomic level was suddenly shattered."
>
> >http://www.stanford.edu/class/cs273a/papers.aut07/lecture5/cnvOpinion...
>
> Have you factored in the CNV differences between a given human and a
> given chimp?
Again, given your above denials of my interpretation of your arguments
thus far, what's your point here? How do you overcome the
interpretation of many mainstream scientists, perhaps most now, that
the notion that any two humans were more than 99.7 % identical (less
than 10 million base differences) at the genomic level is now
"suddenly shattered"?
Sean Pitman
www.DetectingDesign.com
seanpi...@naturalselection.0catch.com
wrote:
> John S. Wilkins wrote:
Like I said, mainstream scientists use all kinds of definitions for
"species" and call each other "fringe" when their pet definitions
clash.
> > Moreover, barcoding is getting government funding (which pisses me off
> > no end as it seems to be largely driven by a single company) as a
> > replacement for field taxonomy and ecology. It's a technosolution to a
> > problem that is multivariate and costly, so of course bureaucrats love
> > it.
>
> Let's not start trading barcoding rants.
>
> > There are definitions of "species" that rely on molecular clustering
> > (e.g., Jim Mallet's, and possibly Templeton's suitably interpreted)
> > although some earlier ones (e.g., Cracraft's and Eldredge's) had talked
> > about diagnosable clusters of individuals' traits.
>
> If you actually look at what Mallet says, he also requires that these
> clusters be stable in sympatry; i.e. it's a disguised form of the BSC.
In any case, what is your reproducible, practical definition of a
"species"?
Sean Pitman
www.DetectingDesign.com