Creationism Question (may be old business)
JTEM
So everyone accepts microevolution, even the luniest
of the lunatic creationists.
What makes it stop?
They accept this "microevolution" can produce all the
differences we see in Great Danes & Chihuahuas
(Greyhounds & Dachshunds), but what is it that they
claim makes this so-called "Process" stop creating
such differences? I'll explain.
When were dogs first domesticated?
That's a rhetorical question. The actual answer isn't
that important. Say it was 6,000 years ago, or
14,000 or even 100,000 -- it really doesn't matter.
Pick whatever figure you're happy with, take note
of all the different breeds of dogs with all their
different traits which have arisen in that time, and then
multiply the figure by ten.
Example: If you want to say that dogs were first
domesticated 100,000 years ago -- given that
"microevolution" you accept having produced all
the different breeds with all their different traits
over that 100,000 year period, what stops that same
evolution from producing twice the differences in
200,000 years.... 10 times the differences in a
million years?
It just seems to me that once you accept
"microevolution" -- which even the craziest wingnut
does -- unless you're also proposing some
mechanism for shutting it off, you have no choice
but to accept that, at some point, the inescapable
result is going to be a new species that doesn't
resemble the original species in any way. And that
eventual new species, barring extinction, is going
to do the same -- give rise to a microevolutionary
line that will eventually lead to a new species which
in no way resembles it.
So, of course, creationists (even those known as
I.D.iots) require a mechinism for stopping
microevolution -- for turning it off. They need it. It
is something they must have.
What is it?
Radix2
You calculation is probably conservative, as it may be only in the last
few(?) thousand years that there appears to be a concerted effort to
make new breeds. I fully admit that that is an assertion without
evidence on my behalf but look what just 50 years of intensive
artificial selection did for the Russian Silver Fox
(http://en.wikipedia.org/wiki/Tame_Silver_Fox). There is a link there
to a paper discussing the gene expression differences. which appear
quite substantial. Not only that, but the selective pressure applied
was just to strengthen inherent tameness. Their overall behavior
changed as well as *physiology* and *morphology* What differences
would occur after 200000 years of intense selective pressure.
clyde...@gmail.com
For YECers, time, to the tune of 6000 years. And neither of their 2
Genesis fairy tales describe speciation this way, so it's wrong no
matter what.
For the rest, their incredulity. I've seen some argue that there is a
"species barrier" of some sort, kind of a god-made anti-Darwinian force
field I guess. I don't know where they come up with that, but
hopefully one will respond and describe this phenomenon. But on the
whole, OECers and IDiots just argue from incredulity: that it's not
probable, there's not enough evidence, it defies reason, the molecular
evidence shows that some mechanisms couldn't evolve, design makes more
sense, etc.
Bobby Bryant
"JTEM" <jte...@gmail.com> writes:
>
> So everyone accepts microevolution, even the luniest
> of the lunatic creationists.
Possibly not _everyone_.
> What makes it stop?
God steps in at some point, and says "Illdoit".
--
Bobby Bryant
Reno, Nevada
Remove your hat to reply by e-mail.
Victor Eijkhout
> It just seems to me that once you accept
> "microevolution" -- which even the craziest wingnut
> does -- unless you're also proposing some
> mechanism for shutting it off,
Nah. It's obvious.
I accept the idea of jumping up by a short distance. Me, I barely clear
a meter, but my brother gets a couple of feet more. The record is over 2
meter, and if you use a pole you can get even higher.
But I need no mechanism to be able to claim that no one will ever jump
to the moon. No amount of micro-jumping will ever get you to that macro
amount.
Victor.
--
Victor Eijkhout -- eijkhout at tacc utexas edu
Martin Andersen
What a nice false analogy.
I'm curious, are you also in denial of lunar landings? Because, you know, we
didn't get there by cannon.
Clyde Squid
On Dec 28, 1:09 pm, s...@sig.for.address (Victor Eijkhout) wrote:
> JTEM <jte...@gmail.com> wrote:
> > It just seems to me that once you accept
> > "microevolution" -- which even the craziest wingnut
> > does -- unless you're also proposing some
> > mechanism for shutting it off,Nah. It's obvious.
>
> I accept the idea of jumping up by a short distance. Me, I barely clear
> a meter, but my brother gets a couple of feet more. The record is over 2
> meter, and if you use a pole you can get even higher.
>
> But I need no mechanism to be able to claim that no one will ever jump
> to the moon. No amount of micro-jumping will ever get you to that macro
> amount.
>
> Victor.
> --
> Victor Eijkhout -- eijkhout at tacc utexas edu
Bad analogy. The question was why some believe that successive changes
in a population can't result in a new species. One cannot successively
jump up higher and higher, so you're not really answering the question.
A better analogy would be that I cannot jump from where I am in
central Alabama to Mississippi...in one jump. However, I could jump
there little by little. The question raised is why creationists accept
that I can make tiny jumps towards Mississippi, but deny that I could
ever change states.
At least, that's how I interpret the question.
Victor Eijkhout
> A better analogy would be that I cannot jump from where I am in
> central Alabama to Mississippi...in one jump. However, I could jump
> there little by little.
Nice improvement on my (obviously crappy; would the other respondent
please evolve a sense of humour?) analogy.
Seanpit
The analogy really isn't so bad. It's pretty good actually.
The problem is that not all types of functions that are present within
biosystems are created equal. Different types of functions require
different minimum size and specificity structural requirements. Some
functions only require a few residues while others require many
specifically arranged residue structural "parts" in order for a
particular function to work - even a little bit.
Evolving low-level functions is kinda like finding a meaningful
3-letter character sequence in the English language system. It is
fairly easy to do because the ratio of potentially
meaningful/beneficial vs. non-beneficial sequences is relatively high
(about 1 in 18 or so). However, this ratio drops exponentially when it
comes to finding higher and higher level functions. For example, the
ratio of potentially beneficial vs. non-beneficial 7-character
sequences drops to less than 1 in 250,000.
So, you see, it gets exponentially harder and harder to keep jumping up
to the next higher level of functions with greater minimum size and/or
specificity requirements. This means that exponentially more and more
time is required to cross the gap between what is and what might be
beneficial at higher and higher functional levels. Very quickly
trillions upon trillions of years of time, on average, are required to
evolve any novel beneficial function at the next higher level.
Consider that novel low level functions, those functions that require
less than 100 fairly specified residues, evolve on a fairly regular
basis in a wide variety of living organisms. However, those functions
that require at least 3 to 5 hundred residues are much more difficult
to evolve and are usually limited to a single type of organism with
specific features (like very fortuitous starting points). Now, note
that no functions that require at least 1000 specifically arranged
residues ever evolve. There isn't a single documented case in all of
scientific literature.
This observation of the stalling out of evolutionary potential is a
fact that is clearly documented. The obvious reason for this stalling
out effect is due to the exponential expansion of the non-beneficial
gap problem. The only means of getting across this gap is random
mutation. Natural selection is helpless because nature can only
select, in a positive way, those mutations that result in some
functional improvement over what came before. Stepping from an island
of beneficial function into the non-beneficial gap that exists between
high-level functions is a detrimental step, from the perspective of
natural selection. Therefore, nature will select to remove that
mutational sequence from the gene pool. Sometimes a sequence may be
allowed to undergo random walk for a while within the gap, but both
random walk and random mutational steps of any size have approximately
the same likelihood of finding a novel beneficial sequence within the
vast potential of sequence space (exponentially more vast with each
additional minimum size requirement).
In the end, jumping farther into the non-beneficial gap doesn't improve
the odds of success and evolutionary processes stall out completely on
very low rungs of the ladder.
Sean Pitman
www.DetectingDesign.com
bi...@juno.com
>>
> So, of course, creationists (even those known as
> I.D.iots) require a mechinism for stopping
> microevolution -- for turning it off. They need it. It
> is something they must have.
>
> What is it?
I'm not certain. But I bet it is similar to the mechanism that prevents
a mule from reproducing. When two separate species (horse and donkey)
breed, they are able to reproduce, but their offspring is sterile.
If two species breed and produce offspring that is sterile, this won't
lead to any further "evolution."
Now, if we take it down to the DNA level, I have a feeling that some
so-called "junk DNA" segments prevent speciation. The more we discover
about the "junk DNA" the less likely evolution will become, I'll wager.
Something happens during the meiosis of donkey-horse breeding that
prevents the offspring from being fertile. I have a suspicion that this
would occur in every case, and thus macro-evolution is DOA.
Free Lunch
bi...@juno.com wrote in
<1167345302.2...@a3g2000cwd.googlegroups.com>:
>
>>>
>> So, of course, creationists (even those known as
>> I.D.iots) require a mechinism for stopping
>> microevolution -- for turning it off. They need it. It
>> is something they must have.
>>
>> What is it?
>
>I'm not certain. But I bet it is similar to the mechanism that prevents
>a mule from reproducing. When two separate species (horse and donkey)
>breed, they are able to reproduce, but their offspring is sterile.
>
>If two species breed and produce offspring that is sterile, this won't
>lead to any further "evolution."
>
>Now, if we take it down to the DNA level, I have a feeling that some
>so-called "junk DNA" segments prevent speciation.
What scientific evidence supports your speculation?
>The more we discover
>about the "junk DNA" the less likely evolution will become, I'll wager.
So far all of the discoveries have supported evolution. What causes you
to assert that the discoveries in the future will be different?
>Something happens during the meiosis of donkey-horse breeding that
>prevents the offspring from being fertile. I have a suspicion that this
>would occur in every case, and thus macro-evolution is DOA.
It appears that you don't understand what happens in evolution or the
breeding of mules.
Clyde Squid
On Dec 28, 4:02 pm, "Seanpit"
<seanpitnos...@naturalselection.0catch.com> wrote:
> Clyde Squid wrote:
> > On Dec 28, 1:09 pm, s...@sig.for.address (Victor Eijkhout) wrote:
> > > JTEM <jte...@gmail.com> wrote:
> > > > It just seems to me that once you accept
> > > > "microevolution" -- which even the craziest wingnut
> > > > does -- unless you're also proposing some
> > > > mechanism for shutting it off,Nah. It's obvious.
>
> > > I accept the idea of jumping up by a short distance. Me, I barely clear
> > > a meter, but my brother gets a couple of feet more. The record is over 2
> > > meter, and if you use a pole you can get even higher.
>
> > > But I need no mechanism to be able to claim that no one will ever jump
> > > to the moon. No amount of micro-jumping will ever get you to that macro
> > > amount.
>
> > > Victor.
> > > --
> > > Victor Eijkhout -- eijkhout at tacc utexas edu
>
> > Bad analogy. The question was why some believe that successive changes
> > in a population can't result in a new species. One cannot successively
> > jump up higher and higher, so you're not really answering the question.
> > A better analogy would be that I cannot jump from where I am in
> > central Alabama to Mississippi...in one jump. However, I could jump
> > there little by little. The question raised is why creationists accept
> > that I can make tiny jumps towards Mississippi, but deny that I could
> > ever change states. At least, that's how I interpret the question.The analogy really isn't so bad. It's pretty good actually.
>
> The problem is that not all types of functions that are present within
> biosystems are created equal. Different types of functions require
> different minimum size and specificity structural requirements. Some
> functions only require a few residues while others require many
> specifically arranged residue structural "parts" in order for a
> particular function to work - even a little bit.
What functions are you talking about? What are "parts" in your world?
> Evolving low-level functions is kinda like finding a meaningful
> 3-letter character sequence in the English language system. It is
> fairly easy to do because the ratio of potentially
> meaningful/beneficial vs. non-beneficial sequences is relatively high
> (about 1 in 18 or so).
Wow, look, numbers. Where did they come from?
However, this ratio drops exponentially when it
> comes to finding higher and higher level functions. For example, the
> ratio of potentially beneficial vs. non-beneficial 7-character
> sequences drops to less than 1 in 250,000.
I don't know where you are getting these numbers, but I strongly
suspect that they are total crap. If you wish me to think otherwise,
source please.
>
> So, you see, it gets exponentially harder and harder to keep jumping up
> to the next higher level of functions with greater minimum size and/or
> specificity requirements.
Not really. Look into developmental biology. Small changes in genes
can result in very selectable differences in developmental patterns.
>This means that exponentially more and more
> time is required to cross the gap between what is and what might be
> beneficial at higher and higher functional levels. Very quickly
> trillions upon trillions of years of time, on average, are required to
> evolve any novel beneficial function at the next higher level.
What peer-reviewed papers can I read that discuss this "gap" of yours
in greater detail. I would love to read them. I don't see the math,
and I doubt your numbers. Citation please.
>
> Consider that novel low level functions, those functions that require
> less than 100 fairly specified residues, evolve on a fairly regular
> basis in a wide variety of living organisms. However, those functions
> that require at least 3 to 5 hundred residues are much more difficult
> to evolve and are usually limited to a single type of organism with
> specific features (like very fortuitous starting points). Now, note
> that no functions that require at least 1000 specifically arranged
> residues ever evolve. There isn't a single documented case in all of
> scientific literature.
I'm sorry, but this makes no sense. Your terminology is unclear, and I
gather that's intentional. When you say residue, do you mean amino
acid? And what it is a "novel low level function.?" And this whole
1000 specifically arranged residues thing, I'm not buying it. I'm not
saying I won't, it's just that you are not being in the least bit
clear. Try again, this time with sources.
> This observation of the stalling out of evolutionary potential is a
> fact that is clearly documented. The obvious reason for this stalling
> out effect is due to the exponential expansion of the non-beneficial
> gap problem. The only means of getting across this gap is random
> mutation. Natural selection is helpless because nature can only
> select, in a positive way, those mutations that result in some
> functional improvement over what came before. Stepping from an island
> of beneficial function into the non-beneficial gap that exists between
> high-level functions is a detrimental step, from the perspective of
> natural selection. Therefore, nature will select to remove that
> mutational sequence from the gene pool. Sometimes a sequence may be
> allowed to undergo random walk for a while within the gap, but both
> random walk and random mutational steps of any size have approximately
> the same likelihood of finding a novel beneficial sequence within the
> vast potential of sequence space (exponentially more vast with each
> additional minimum size requirement).
No one has observed evolution stalling out. You are now just stating
that things can't happen based on nothing more than your own personal
wishes. You have failed to make an argument for anything, as your
words are unclear, your numbers unsubstantiated, and your conclusions
therefore baseless. And you have yet to propose what did happen. Puff
of smoke?
When are you ID people going to stop trying to prove that evolution
didn't do it and start getting around to providing evidence for what
did happen? Positive evidences? Unqualified numbers used to show what
you think didn't happen doesn't impress me or anybody else.
> In the end, jumping farther into the non-beneficial gap doesn't improve
> the odds of success and evolutionary processes stall out completely on
> very low rungs of the ladder.
You have failed to show that such a gap exists, failed to provide any
way for us to check your math, and failed to show you reached your
conclusion by any means other than whispers from the gods. Please work
on this.
> Sean Pitmanwww.DetectingDesign.com
Clyde
Mark VandeWettering
>
>>>
>> So, of course, creationists (even those known as
>> I.D.iots) require a mechinism for stopping
>> microevolution -- for turning it off. They need it. It
>> is something they must have.
>>
>> What is it?
>
> I'm not certain. But I bet it is similar to the mechanism that prevents
> a mule from reproducing. When two separate species (horse and donkey)
> breed, they are able to reproduce, but their offspring is sterile.
>
> If two species breed and produce offspring that is sterile, this won't
> lead to any further "evolution."
So, how is it that these two species can reproduce at all? You've admitted
that horses and donkeys are separate species, why can they even produce
mules?
Doesn't that question trouble you? Or is it simply a case of "no brains,
no pains"?
> Now, if we take it down to the DNA level, I have a feeling that some
> so-called "junk DNA" segments prevent speciation. The more we discover
> about the "junk DNA" the less likely evolution will become, I'll wager.
Don't bet more than you can afford to lose.
> Something happens during the meiosis of donkey-horse breeding that
> prevents the offspring from being fertile. I have a suspicion that this
> would occur in every case, and thus macro-evolution is DOA.
And denial is a river in egypt.
Mark
Ernest Major
<lu...@nofreelunch.us> writes
>>Now, if we take it down to the DNA level, I have a feeling that some
>>so-called "junk DNA" segments prevent speciation.
>
>What scientific evidence supports your speculation?
On the other hand, it seems to me that the existence of junk DNA assists
speciation - in the absence of purifying selection junk DNA accumulates
differences (between isolated populations) faster than non-junk DNA, and
therefore contributes disproportionately to the development of the
post-zygotic isolating mechanism of hybrid infertility due to meiotic
disruption; not to mention the likely positive effects on fertility of
transposon activation in (some) neopolyploids through the suppression of
polyvalent formation.
--
alias Ernest Major
John Harshman
>>So, of course, creationists (even those known as
>>I.D.iots) require a mechinism for stopping
>>microevolution -- for turning it off. They need it. It
>>is something they must have.
>>
>>What is it?
>
>
> I'm not certain. But I bet it is similar to the mechanism that prevents
> a mule from reproducing. When two separate species (horse and donkey)
> breed, they are able to reproduce, but their offspring is sterile.
You lose your bet. The inability of different species to hybridize has
nothing to do with the ability of species to evolve new characteristics,
or to split into multiple species. If you disagree, present some reason
for there to be a connection.
> If two species breed and produce offspring that is sterile, this won't
> lead to any further "evolution."
>
> Now, if we take it down to the DNA level, I have a feeling that some
> so-called "junk DNA" segments prevent speciation. The more we discover
> about the "junk DNA" the less likely evolution will become, I'll wager.
How would these junk DNA segments act to prevent speciation? And is your
"feeling" based on anything other than your desire for there to be a
mechanism somewhere?
> Something happens during the meiosis of donkey-horse breeding that
> prevents the offspring from being fertile. I have a suspicion that this
> would occur in every case, and thus macro-evolution is DOA.
Again a non sequitur. Even if your suspicion were true, how does the
inability of separate species to hybridize prevent either evolution or
speciation? This requires a strawman view of speciation, in which it's
caused by a single macromutation to an individual, rather than a series
of small mutations and fixations within populations.
Marc
> Clyde Squid wrote:
................ snip #1
> So, you see, it gets exponentially harder and harder to keep jumping up
> to the next higher level of functions with greater minimum size and/or
> specificity requirements. This means that exponentially more and more
> time is required to cross the gap between what is and what might be
> beneficial at higher and higher functional levels.
"Exponential", Sean? Are you out to impress here?
> Very quickly
> trillions upon trillions of years of time, on average, are required to
> evolve any novel beneficial function at the next higher level.
Oh My gOd, YES... The "Average of Trillions of Years" impressive
make-believe number system is still your most impressive statement.
(Shame that it is just make-believe.)
> Consider that novel low level functions, those functions that require
> less than 100 fairly specified residues, evolve on a fairly regular
> basis in a wide variety of living organisms. However, those functions
> that require at least 3 to 5 hundred residues are much more difficult
> to evolve and are usually limited to a single type of organism with
> specific features (like very fortuitous starting points). Now, note
> that no functions that require at least 1000 specifically arranged
> residues ever evolve. There isn't a single documented case in all of
> scientific literature.
.................................. snip #2...
Somehow you failed to reply a couple of months ago about the (then)
recent biomedical literature on gene duplication. Of course, you had
also failed to reply a few months before that on the (then) very recent
literature, and you ignored my posts from many months ago about
gene duplication in general, and also ignored domain shuffling and
other aspects of evolution that provide the mechanism of larger size
segments being brought together. You _did_ say a couple of times
that "duplication just provides more of the same" and not any sort
of new function. That is, of course, quite wrong - as you have been
told by myself and others - but you, of course, ignore that.
In my Nov 21 post in the "What do you know that the rest of the
world doesn't" thread, I point out that several of the then new cites
use phrases like "gene duplication is a major force in evolution".
You're entire premise about complexity falls apart when you take
duplication on board, doesn't it Sean? I have shown myself able to
learn things - accepting that transmissible tumours are a form of
evolution - so how about _you_ accepting when you are wrong and
adjusting your model. Silly overstatements about "trillions" of years
(in a universe that is 0.014 trillion years old) are just there to try
to impress the odd lurker who finds your posts clearly written, but
no matter how clearly you write garbage, it is still garbage. Ignore
the duplication literature again and again, and every couple of months
there will be a couple of dozen new reports that *ALL* disagree with
the statements that you are making. When will you be able to admit
this, Sean? Perhaps reading some of the papers would be good. My
offer to send you PDFs of papers you have trouble getting is still
open.
A search of PubMed (www.pubmed.gov) for gene duplication today
gives 4971 hits - there were 4891 back on Nov. 21st - so let's look
at the eighty *NEW* reports about "gene duplication", shall we?
I won't cite most of the 80 new reports but please review them, as
I have, to see if any of them disagree with the examples I will cite.
Note to Lurkers and other readers - to get author names, the full
abstract (I will just quote a bit from selected abstracts) and such,
go to www.pubmed.gov and enter the PMID number for a citation.
When these are available in free, full text, the link is given below.
"Divergence of protein kinase A catalytic subunits in Cryptococcus
neoformans and Cryptococcus gattii illustrates evolutionary
reconfiguration of a signaling cascade." Eukaryot Cell. 2006
Dec 22; [Epub ahead of print] PMID: 17189488
The abstract begins: "Gene duplication and divergence via both loss
and gain of gene activities are powerful evolutionary forces underlying
the origin of new biological functions."
"Robustness and evolvability in genetic regulatory networks."
J Theor Biol. 2006 Nov 1; [Epub ahead of print] PMID: 17188715
"The evolution of Mammalian gene families."
PLoS ONE. 2006 Dec 20;1:e85. PMID: 17183716
Abstract: Gene families are groups of homologous genes that are likely
to have highly similar functions. Differences in family size due to
lineage-specific gene duplication and gene loss may provide clues to
the evolutionary forces that have shaped mammalian genomes. Here we
analyze the gene families contained within the whole genomes of human,
chimpanzee, mouse, rat, and dog. In total we find that more than half
of the 9,990 families present in the mammalian common ancestor have
either expanded or contracted along at least one lineage. Additionally,
we find that a large number of families are completely lost from one or
more mammalian genomes, and a similar number of gene families have
arisen subsequent to the mammalian common ancestor. Along the lineage
leading to modern humans we infer the gain of 689 genes and the loss of
86 genes since the split from chimpanzees, including changes likely
driven by adaptive natural selection. Our results imply that humans and
chimpanzees differ by at least 6% (1,418 of 22,000 genes) in their
complement of genes, which stands in stark contrast to the oft-cited
1.5% difference between orthologous nucleotide sequences. This genomic
"revolving door" of gene gain and loss represents a large number of
genetic differences separating humans from our closest relatives.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17183716
"Not Born Equal: Increased Rate Asymmetry in Relocated and
Retrotransposed Rodent Gene Duplicates."
Mol Biol Evol. 2006 Dec 18; [Epub ahead of print] PMID: 17179139
Abstract: Duplicated genes frequently evolve at different rates. This
asymmetry is evidence of natural selection's ability to discriminate
between the two copies, subjecting them to different levels of
purifying selection, or even permitting adaptive evolution of one or
both copies. However, if gene duplication creates pairs of protein
coding sequences that are initially identical, this raises the question
of how selection tells the two copies apart. Here we investigated
asymmetric sequence divergence of recently duplicated genes in rodents
and related this to two possible sources of such asymmetry: gene
relocation as a consequence of duplication, and retrotransposition as a
mechanism of gene duplication. We found that most young rodent
duplicates that have been relocated were created by retrotransposition.
The degree of rate asymmetry in gene pairs where one copy has been
relocated (either by retrotransposition or DNA-based duplication) is
greater than in pairs formed by local DNA-based duplication events.
Furthermore, by considering the direction of transposition for distant
duplicates, we found a consistent tendency for retrogenes to undergo
accelerated protein evolution relative to their static paralogs,
whereas DNA-based transpositions showed no such tendency. Finally, we
demonstrate that the faster sequence evolution of retrogenes correlates
with the profound alteration of their expression pattern that is
precipitated by retrotransposition.
NOTE - Sean, do you still deny that transposons move genes
around? Here they show that this also allows for faster protein
evolution, but you keep saying that the duplicated genes remain
the same. What say you now?
"Evidence of Interaction Network Evolution by Whole Genome
Duplications: a Case-study in MADS-box Proteins."
Mol Biol Evol. 2006 Dec 14; [Epub ahead of print] PMID: 17175526
(This abstract is well worth reading....)
"Comparative and phylogenetic analysis of alpha-l-fucosidase genes."
Gene. 2006 Nov 11; [Epub ahead of print] PMID: 17175120
"Evolution of secretin family GPCR members in the metazoa."
BMC Evol Biol. 2006 Dec 13;6(1):108 [Epub...] PMID: 17166275
>From the abstract: "The family 2 GPCR members provide a good
example of gene duplication events occurring in tandem with
increasing organismal complexity during metazoan evolution."
Link to full text - http://www.biomedcentral.com/1471-2148/6/108
"Catalytic activity, duplication and evolution of the CYP98
cytochrome P450 family in wheat." Plant Mol Biol. 2007
Jan;63(1):1-19. Epub 2006 Nov 25. PMID: 17160453
The abstract starts: "A burst of evolutionary duplication upon
land colonization seems to have led to the large superfamily
of cytochromes P450 in higher plants. Within this superfamily
some clans and families are heavily duplicated."
"Evolution of the Metazoan Protein Phosphatase 2C Superfamily."
J Mol Evol. 2007 Jan;64(1):61-70. Epub 2006 Dec 6. PMID: 17160364
>From the abstract: "The phylogeny of PP2C was reconstructed,
revealing the existence of 15 vertebrate families which arose
following a series of gene duplication events. Relative dating
of these duplications showed that they occurred in two active
periods: before the divergence of bilaterians and before vertebrate
diversification."
"Functional analysis of gene duplications in Saccharomyces cerevisiae."
Genetics. 2006 Dec 6; [Epub ahead of print] PMID: 17151249
http://www.genetics.org/cgi/rapidpdf/genetics.106.064329v1
"Almost all human genes resulted from ancient duplication."
Proc Natl Acad Sci U S A. 2006 Dec 12;103(50):19027-32.
Epub 2006 Dec 4. PMID: 17146051 (This says it all...)
"Mechanisms and Rates of Birth and Death of Dispersed
Duplicated Genes During the Evolution of a Multigene Family
in Diploid and Tetraploid Wheats." Mol Biol Evol. 2006
Nov 29; [Epub ahead of print] PMID: 17135334
The abstract ends: "The half-life of ALP duplicated genes was
estimated to be 0.87 MY. Strong purifying selection acting on
the ancestral gene ALP-A1 was undiminished by the evolution
of duplicated genes. The evolution of the ALP family shows
that repeated elements facilitate both gene duplication and
expression of duplicated genes and highlights their importance
for the evolution of gene repertoire in large plant genomes."
"Functional Diversification of B MADS-Box Homeotic Regulators
of Flower Development: Adaptive Evolution in Protein-Protein
Interaction Domains After Major Gene Duplication Events."
Mol Biol Evol. 2006 Nov 29; [Epub ...] PMID: 17135333
The abstract ends: "We thus propose a mechanism of functional
diversification and persistence of gene duplicates by the
appearance of novel multimerization capabilities after duplications.
Multimer formation in different combinations of regulatory proteins
can be a mechanistic basis for the origin of novel regulatory
functions and a gene regulatory mechanism for the appearance
of morphological innovations.
"Evolution of plant microRNA gene families." Cell Res. 2006
Nov 28; [Epub ahead of print] PMID: 17130846
"Multiple Gene Duplication and Rapid Evolution in the groEL
Gene: Functional Implications." J Mol Evol. 2006
Dec;63(6):781-7. Epub 2006 Nov 10. PMID: 17103057
The abstract: "Gene duplication is one of the most important mechanisms
for creating new genes and generating genomic novelty.
Retrotransposon-mediated sequence transduction (i.e., the process by
which a retrotransposon carries flanking sequence during its
mobilization) has been proposed as a gene duplication mechanism. L1
exon shuffling potential has been reported in cell culture assays, and
two potential L1-mediated exon shuffling events have been identified in
the genome. SVA is the youngest retrotransposon family in primates and
is capable of 3' flanking sequence transduction during
retrotransposition. In this study, we examined all of the full-length
SVA elements in the human genome to assess the frequency and impact of
SVA-mediated 3' sequence transduction. Our results showed that
approximately 53 kb of genomic sequences have been duplicated by 143
different SVA-mediated transduction events. In particular, we
identified one group of SVA elements that duplicated the entire AMAC
gene three times in the human genome through SVA-mediated transduction
events, which happened before the divergence of humans and African
great apes. In addition to the original AMAC gene, the three transduced
AMAC copies contain intact ORFs in the human genome, and at least two
are actively transcribed in different human tissues. The duplication of
entire genes and the creation of previously undescribed gene families
through retrotransposon-mediated sequence transduction represent an
important mechanism by which mobile elements impact their host
genomes."
"Adaptive evolution of Hox-gene homeodomains after cluster
duplications."
BMC Evol Biol. 2006 Nov 1;6:86. PMID: 17078881
http://www.biomedcentral.com/1471-2148/6/86
"Comparative genomics of vertebrate Fox cluster loci."
BMC Genomics. 2006 Oct 24;7:271. PMID: 17062144
The abstract starts: "BACKGROUND: Vertebrate genomes contain
numerous duplicate genes, many of which are organised into paralagous
regions indicating duplication of linked groups of genes. Comparison
of genomic organisation in different lineages can often allow the
evolutionary history of such regions to be traced."
http://www.biomedcentral.com/1471-2164/7/271
Sean will no doubt mutter something about these reports all
being "just-so stories" and such, but that is such a big cop-out.
C'mon, Sean... learn a little, accept that these reports are most
likely all completely factual and it (again) kills off your "theory"
about the impossibility of complexity arising.
(signed) marc
..
Pithecanthropus Erectus
Victor was being facetious without attributions.
--
And yeah, a great way to marginalize creationists is to use their idiocy
to highlight the weaknesses of religion, and draw people away from the
churchly hothouse that fosters that kind of damned dumb thinking.
Meanwhile, some people make excuses for the source of our nation's curse
and beg us not to pick on poor, blameless religion, because that will
antagonize people.
Tough.
PZ Myers
Pharyngula Blog, 12/26/2006
Pithecanthropus Erectus
Macro evolution is not about hybridization. The reason behind the
inability to produce fertile offspring when species are merged through
hybridizing is well understood.
Genetic modifications and random selection are also well understood, and
completely separate processes. If you didn't spend so much time trying
to twist yourself around to fight evolution and read even basic articles
on the process, you would be able to understand it.
Do you propose in your voucher funded schools to teach genetics
incorrectly just to hide the facts of evolution from the kids?
Marc
Seanpit wrote:
.................. ....... snp
.... the link to an earlier thread I gave seems to point to
the reply to my post and not to my post itself.
The thread I tried to cite in the reply above is
http://groups.google.com/group/talk.origins/browse_frm/thread/a93ec2f313c3560f/#
The message I wrote to Sean with the list of citations was on Nov 21
(of course, he didn't read those and he most likely won't read the
current ones cited in my other reply here... but to show Lurkers and
other readers the information Sean ignores, I'm still happy to look
through these abstracts)
(signed) marc
.
JTEM
Victor Eijkhout wrote:
> Nah. It's obvious.
>
> I accept the idea of jumping up by a short distance. Me,
> I barely clear a meter, but my brother gets a couple of
> feet more. The record is over 2 meter, and if you use a
> pole you can get even higher.
>
> But I need no mechanism to be able to claim that no
> one will ever jump to the moon. No amount of micro-jumping
> will ever get you to that macro amount.
I sincerely hope that you're trolling, as what you describe
is hardly analogous to what creationism requires, and is
also clearly wrong.
There is a "mechanism" of sorts that stops you from
jumping to the moon. It's called "Gravity," and it pulls
you back down to the earth.
Secondly, successive jumps to not begin at the height
achieved by the previous jump, while microevolutionary
changes clearly do build on each previous change.
JTEM
Seanpit wrote:
> The analogy really isn't so bad. It's pretty good
> actually.
....NOT!
JTEM
bi...@juno.com wrote:
> When two separate species (horse and donkey)
> breed, they are able to reproduce, but their
> offspring is sterile.
As others have pointed out, that's quite irrelevant unless
you want to pretend that microevolution results from
two different species interbreeding.
> If two species breed and produce offspring that is
> sterile, this won't lead to any further "evolution."
So? It's irrelevant to the question.
> Now, if we take it down to the DNA level, I have a
> feeling that some so-called "junk DNA" segments
> prevent speciation.
How? Why?
Steven J.
JTEM wrote:
> So everyone accepts microevolution, even the luniest
> of the lunatic creationists.
>
> What makes it stop?
>
answer a creationist could give you. One of the earliest criticisms of
gradualism and natural selection was the idea that the earliest stage
of a complex adaption would, necessarily, be useless (you see this in
the common "what good is 1% of an eye" argument, but there are also
"what good is 1% of a leg, heart, liver, etc." arguments. You could
view a "created kind" (or at least the potential for "microevolution"
of a "created kind") as a bubbleful of phenotypes (within some
morphological hyperspace; I should probably have stuck with the more
familiar "genetic space," but, after all, living things require actual
bodies, not just genomes) each of which is viable in some plausible
environment, surrounded by a sea of phenotypes that are not viable in
any plausible environment. There are, of course, a great many such
"bubbles" in the space of all possible life forms, but the space
between them is impassable by small, nonmiraculous steps, because any
intermediate form that ended up in the sea between the bubbles would be
unable to survive.
>
> They accept this "microevolution" can produce all the
> differences we see in Great Danes & Chihuahuas
> (Greyhounds & Dachshunds), but what is it that they
> claim makes this so-called "Process" stop creating
> such differences? I'll explain.
>
> When were dogs first domesticated?
>
> That's a rhetorical question. The actual answer isn't
> that important. Say it was 6,000 years ago, or
> 14,000 or even 100,000 -- it really doesn't matter.
> Pick whatever figure you're happy with, take note
> of all the different breeds of dogs with all their
> different traits which have arisen in that time, and then
> multiply the figure by ten.
>
> Example: If you want to say that dogs were first
> domesticated 100,000 years ago -- given that
> "microevolution" you accept having produced all
> the different breeds with all their different traits
> over that 100,000 year period, what stops that same
> evolution from producing twice the differences in
> 200,000 years.... 10 times the differences in a
> million years?
>
do young-earth creationists (e.g. most YECs -- with some amusing
exceptions -- accept "Java man" as "fully human," while Hugh Ross
doesn't even accept the Neanderthals as such).
>
> It just seems to me that once you accept
> "microevolution" -- which even the craziest wingnut
> does -- unless you're also proposing some
> mechanism for shutting it off, you have no choice
> but to accept that, at some point, the inescapable
> result is going to be a new species that doesn't
> resemble the original species in any way. And that
> eventual new species, barring extinction, is going
> to do the same -- give rise to a microevolutionary
> line that will eventually lead to a new species which
> in no way resembles it.
>
> So, of course, creationists (even those known as
> I.D.iots) require a mechinism for stopping
> microevolution -- for turning it off. They need it. It
> is something they must have.
>
> What is it?
-- Steven J.
Iain
Once you've observed the weather, you've also observed the climate.
They are not two seperate things.
It's a joke -- Micro-\Macro just refer to different orders of
magnitude, that's all.
~Iain
Blodgett
> This observation of the stalling out of evolutionary potential is a
> fact that is clearly documented.
You must be one of those people who think that all life-forms are
"perfect" for their environment. We know that most evolutionary change
comes not from mutation but change in population and therefore
expression of genes.
I think Sean's explanation is an unfortunate mish-mash of misunderstood
information theory (A-la Behe) and wild speculation. From a genertic
point of view, evolution is part down to mutation, but mostly down to
change in population and expression of genes over successive
generations. There is no organism I know of which is not under some
kind of selective pressure, so genes which confer a reproductive
advantage will tend to be selected for.
If creationists had managed to find a life-form with stalled
evolutionary potential (a mumbo-jumbo phrase), it would be an
astonishing discovery. We know that in a stable environment there is
less selective pressure, however this hardly amounts to a "stalling".
> The obvious reason for this stalling
> out effect is due to the exponential expansion of the non-beneficial
> gap problem. The only means of getting across this gap is random
> mutation. Natural selection is helpless because nature can only
> select, in a positive way, those mutations that result in some
> functional improvement over what came before.
This is the usual creationist mistake of assuming that beneficial
mutations are impossible; or that all mutations are either neutral or
non-beneficial.
I think we all accept that there is a process called "evolution" which
was responsible for the differentiation we see in dogs. We have no
reason to suppose that the processes that cause mutation work
differently today than when dogs first became domesticated.
If Sean's argument is to be believed we must accept either that no
mutation can be beneficial or that the environment is incapable of
putting a selective pressure on organisms, and therefore there would be
no reason for one organism to do better than another.
> In the end, jumping farther into the non-beneficial gap doesn't improve
> the odds of success and evolutionary processes stall out completely on
> very low rungs of the ladder.
Again, Sean is imagining evolution like a massive jump. It's more like
a series of very minute jumps some of which lead somewhere interesting
others go absolutely nowhere.
Blodgett
> > What is it?I'm not certain. But I bet it is similar to the mechanism that prevents
> a mule from reproducing. When two separate species (horse and donkey)
> breed, they are able to reproduce, but their offspring is sterile.
No mystery there: A mule is a hybrid between a horse and a donkey.
Those two species have different numbers of chromosomes, so while they
have enough common ancestry to produce an offspring, their reproductive
machinery is broken.
> Something happens during the meiosis of donkey-horse breeding that
> prevents the offspring from being fertile. I have a suspicion that this
> would occur in every case, and thus macro-evolution is DOA.
Again, a typical and almost comical misunderstanding. The existence of
all the species of Equidae which are able to interbreed with different
success is a result of the speciation process. It is commonly accepted
that horses and donkeys have a common ancestor which was neither a
horse, nor a donky but the common progenator of both. Somehow and over
a very long period of time two groups evolved "futher" apart.
Wheras most species cannot interbreed, the fact that horses and donkeys
can produce viable offspring shows that they are genetically very
close. One might even regard these as living fossils that show a
speciation event in process.
Greg G.
But you can't jump from Mississippi to Arkansas because we're all
wicked witches who would melt if we got wet. (For those not familiar
with US geography, the Mississppi River separates AR and MS.)
>
> At least, that's how I interpret the question.
My interpretation of the creationist position.
--
Greg G.
Put on old clothes before you get out the paint brushes.
John Harshman
[I posted this several days ago and it appears to have been lost in the
ozone. Apologies if you see it more than once.]
>> So everyone accepts microevolution, even the luniest
>> of the lunatic creationists.
Not so fast. Most creationists (I wouldn't be confident about all of
them) accept something they call microevolution, but it doesn't
necessarily bear any relationship to what we call microevolution. Often
they accept only recombination among existing alleles in a population,
and reject all natural selection, new mutations, and such. Remember that
creationists spend much of their time arguing against the peppered moth
experiments, and claiming that if natural selection were a real process,
then we ought to kill our neighbors.
>> What makes it stop?
>>
>> They accept this "microevolution" can produce all the
>> differences we see in Great Danes & Chihuahuas
>> (Greyhounds & Dachshunds), but what is it that they
>> claim makes this so-called "Process" stop creating
>> such differences? I'll explain.
It stops when all the existing variation is exhausted, if you believe
that no new variation can arise.
>> When were dogs first domesticated?
>>
>> That's a rhetorical question. The actual answer isn't
>> that important. Say it was 6,000 years ago, or
>> 14,000 or even 100,000 -- it really doesn't matter.
>> Pick whatever figure you're happy with, take note
>> of all the different breeds of dogs with all their
>> different traits which have arisen in that time, and then
>> multiply the figure by ten.
Dogs were obviously created under domestication, in 4004 BC.
>> Example: If you want to say that dogs were first
>> domesticated 100,000 years ago -- given that
>> "microevolution" you accept having produced all
>> the different breeds with all their different traits
>> over that 100,000 year period, what stops that same
>> evolution from producing twice the differences in
>> 200,000 years.... 10 times the differences in a
>> million years?
>>
>> It just seems to me that once you accept
>> "microevolution" -- which even the craziest wingnut
>> does -- unless you're also proposing some
>> mechanism for shutting it off, you have no choice
>> but to accept that, at some point, the inescapable
>> result is going to be a new species that doesn't
>> resemble the original species in any way. And that
>> eventual new species, barring extinction, is going
>> to do the same -- give rise to a microevolutionary
>> line that will eventually lead to a new species which
>> in no way resembles it.
>>
>> So, of course, creationists (even those known as
>> I.D.iots) require a mechinism for stopping
>> microevolution -- for turning it off. They need it. It
>> is something they must have.
>>
>> What is it?
Simple. They don't really accept microevolution. They accept something
much weaker that they choose to call microevolution, just to confuse you.
Seanpit
Blodgett wrote:
> Hi,
>
> > This observation of the stalling out of evolutionary potential is a
> > fact that is clearly documented.
>
> You must be one of those people who think that all life-forms are
> "perfect" for their environment. We know that most evolutionary change
> comes not from mutation but change in population and therefore
> expression of genes.
>
> I think Sean's explanation is an unfortunate mish-mash of misunderstood
> information theory (A-la Behe) and wild speculation. From a genertic
> point of view, evolution is part down to mutation, but mostly down to
> change in population and expression of genes over successive
> generations. There is no organism I know of which is not under some
> kind of selective pressure, so genes which confer a reproductive
> advantage will tend to be selected for.
That's just change within the same gene pool. The gene pool itself
doesn't evolve by such mechanisms. It remains the same. Can't turn a
fish into a mammal this way.
> If creationists had managed to find a life-form with stalled
> evolutionary potential (a mumbo-jumbo phrase), it would be an
> astonishing discovery. We know that in a stable environment there is
> less selective pressure, however this hardly amounts to a "stalling".
Look up the papers by Barry Hall were he does with what he calls
"limited evolutionary potential" of bacteria when it comes to evolving
certain types of functions (like lactase).
> > The obvious reason for this stalling
> > out effect is due to the exponential expansion of the non-beneficial
> > gap problem. The only means of getting across this gap is random
> > mutation. Natural selection is helpless because nature can only
> > select, in a positive way, those mutations that result in some
> > functional improvement over what came before.
>
> This is the usual creationist mistake of assuming that beneficial
> mutations are impossible; or that all mutations are either neutral or
> non-beneficial.
Where did I say that beneficial mutations are impossible? They aren't
impossible. They happen all the time - quite commonly. However, when
they happen they only produce those functions that have very low
minimum size and specificity structural threshold limitations. Higher
and higher level functions are exponentially harder and harder to
evolve. Those functions that require more than 1000 amino acid
residues working together at the same time in fairly specific 3D
orientation never evolve. There isn't a single example in all of
literature.
> I think we all accept that there is a process called "evolution" which
> was responsible for the differentiation we see in dogs.
The differences we see in dogs, cats, horses, pigs, cows, etc., are not
primarily due to evolutionary mechanisms at all - but are largely the
result of Mendelian variation. Mendelian variation is not based on an
evolutionary mechanism. It's completely different. Nothing really
new, as far as the gene pool is concerned, is "evolved" via Mendelian
recombination.
> We have no
> reason to suppose that the processes that cause mutation work
> differently today than when dogs first became domesticated.
Doggy differences aren't based, primarily anyway, on mutations or the
evolution of any novel genetic function within the doggy gene pool.
You need to read up on Mendelian variation a bit more.
> If Sean's argument is to be believed we must accept either that no
> mutation can be beneficial or that the environment is incapable of
> putting a selective pressure on organisms, and therefore there would be
> no reason for one organism to do better than another.
Beneficial mutations do occur and novel functions are evolved via the
stated evolutionary mechanism of random mutation and function-based
selection - just not beyond the lowest levels of functional complexlty.
Hence, the non-beneficial gap problem.
> > In the end, jumping farther into the non-beneficial gap doesn't improve
> > the odds of success and evolutionary processes stall out completely on
> > very low rungs of the ladder.
>
> Again, Sean is imagining evolution like a massive jump. It's more like
> a series of very minute jumps some of which lead somewhere interesting
> others go absolutely nowhere.
The very minute jumps only get you to very low-level functions. Higher
level functions require bigger and bigger jumps because the potential
genetic island sequences coding for potentially beneficial higher-level
functions are exponentially farther and farther appart in sequence
space. You just can't get to a higher level by taking the same size
jump as you did at lower levels.
Sean Pitman
www.DetectingDesign.com
Marc
Seanpit wrote:
> Blodgett wrote:
............................. snp
> Beneficial mutations do occur and novel functions are evolved via the
> stated evolutionary mechanism of random mutation and function-based
> selection - just not beyond the lowest levels of functional complexlty.
> Hence, the non-beneficial gap problem.
.......................... snp
Where do gene duplications fit in the scheme of "random mutations",
Sean?
Please review the recent literature I've cited in this thread (which
builds
on the similar literature cited Nov. 21st and earlier) and indicate how
such driving forces in evolution do not easily cross your imagined gap.
Beside duplications of genes (which clearly lead to novel functions)
there are mechanisms for domain shuffling. What do these do, Sean?
(signed) marc
.
Blodgett
that began this thread:
> > Again, Sean is imagining evolution like a massive jump. It's more like
> > a series of very minute jumps some of which lead somewhere interesting
> > others go absolutely nowhere.The very minute jumps only get you to very low-level functions.
> Higher
> level functions require bigger and bigger jumps because the potential
> genetic island sequences coding for potentially beneficial higher-level
> functions are exponentially farther and farther appart in sequence
> space. You just can't get to a higher level by taking the same size
> jump as you did at lower levels.
I suppose by "higher level function", sean means something like an eye
or a panda's false-thumb. Sean is implicitly making an "irreducable
complexity" argument here because he implies that for this useful
feature to have come about it by evolution it must have come all in one
go, because half a thumb is no good to a panda. He is also stating that
the genetic difference between no false-thumb and having one is far too
big to have occured in a single mutation, which is of course a
straw-man because nobody has ever seriously proposed that.
For us to accept Sean's argument, we would first have to accept Behe's
irreducable complexity. This centeral dogma of modern day creationism
has been widely debunked and has near zero acceptance outside of the ID
/ American fundamentalist community.
"High level functions" might be the combination of a very large number
"low level functions", just like a long meandering walk could be called
a combination of every single little step that took you closer to the
point where you are right now. In order to accept this Behe position
you would have to first believe that little changes cannot add up to
big changes, or you would have to believe that a sequence of small
changes which each have practical benefit cannot exist.
The common rebuttals to Beheism is that co-option, the principle that a
protien that has some apparant function in life today may have been
used differently by the ancestor of that life-form. If you believe in
Beheism you have to believe that cooption is non-existent or somehow
irrelevant.
The great thing is that even IDers have difficulty disputing the notion
that genes which confer some kind of reproductive advantage are
selected for by the environment. If the population of genes are
changing (via what Sean referrs to as Mendellian selection), and the
content of these genes are changing via occasional mutation then you
have every ingredient you need for the kind of very slow, gradual
evolution that I am proposing.
Marc
Marc wrote:
> Seanpit wrote:
> > Clyde Squid wrote:
C'mon Sean - at least have a go at reading these and explaining why
they are not good enough for you to change your thinking.
(signed) marc
sea...@naturalselection.0catch.com
> Marc wrote:
> > Seanpit wrote:
> > > Clyde Squid wrote:
>
> C'mon Sean - at least have a go at reading these and explaining why
> they are not good enough for you to change your thinking.
We've gone over this many times before Marc. These references you list,
which you still haven't read yourself, do nothing more than assume
common decent via gene duplication and mutational divergence, etc.
None of these assumptions has ever been demonstrated when it comes to
producing a novel function that requires more than 1,000 amino acid
residues working together at the same time in a fairly specific 3D
orientation with each other. No such level of functional complexity
ever evolves. There's not a single documented case in all of
literature. Beyond this, none of your papers deal with the statistical
likelihood of any higher level function evolving. The authors simply
assume that it happened based soly on sequence comparisons and the
assumption that similar sequences could only come about via
evolutionary mechanisms of random mutation and function-based
selection.
Sean Pitman
www.DetectingDesign.com
sea...@naturalselection.0catch.com
> Seanpit wrote:
> > Blodgett wrote:
> ............................. snp
>
> > Beneficial mutations do occur and novel functions are evolved via the
> > stated evolutionary mechanism of random mutation and function-based
> > selection - just not beyond the lowest levels of functional complexlty.
> > Hence, the non-beneficial gap problem.
>
> .......................... snp
>
>
> Where do gene duplications fit in the scheme of "random mutations",
> Sean?
Gene duplications are a form of random mutation. However, gene
duplications are no more likely to produce a novel high-level function
that requires a minimum of more than a few thousand specified residues
than is a series of point mutations. You simply don't understand that
the statistics of random selection do not have a significant advantage
over short-step random walk.
> Please review the recent literature I've cited in this thread (which
> builds
> on the similar literature cited Nov. 21st and earlier) and indicate how
> such driving forces in evolution do not easily cross your imagined gap.
Please explain how they do - use some numbers and statistical analysis
here. You've said over and over again that you could and would do
this. I'm waiting . . .
For my part, I've already shown you, over and over again, that gene
duplications do not produce any novel function at all. They just
produce more of the same thing. At this point, you need additional
mutational modifications to achieve a novel function. The number of
random modifications needed at higher levels of functional complexity,
on average, would require trillions upon trillions of years. That's
the problem as I see it. If you disagree, by all means, prove me wrong
. . .
> Beside duplications of genes (which clearly lead to novel functions)
> there are mechanisms for domain shuffling. What do these do, Sean?
Please show me just one example were domain shuffling or gene
duplications of any kind produced a novel function beyond mear
assumption. It just doesn't happen Marc. There isn't such an example
beyond very low levels of functional complexity.
> (signed) marc
Sean Pitman
www.DetectingDesign.com
sea...@naturalselection.0catch.com
Blodgett wrote:
> I think we are getting close to the answer to the original question
> that began this thread:
>
> > > Again, Sean is imagining evolution like a massive jump. It's more like
> > > a series of very minute jumps some of which lead somewhere interesting
> > > others go absolutely nowhere.The very minute jumps only get you to very low-level functions.
>
> > Higher
> > level functions require bigger and bigger jumps because the potential
> > genetic island sequences coding for potentially beneficial higher-level
> > functions are exponentially farther and farther appart in sequence
> > space. You just can't get to a higher level by taking the same size
> > jump as you did at lower levels.
>
> I suppose by "higher level function", sean means something like an eye
> or a panda's false-thumb.
Come on now, why not actually read and at least try to comprehend what
I explained to you twice before? I specifically explained that a the
level of functional complexity I was looking for was one that involved
the production of any novel function that required a minimum threshold
limit of just 1,000 amino acid residues. We aren't talking about
entire organ systems like eyes or thumbs here. Just a relatively
"simple" molecular biosystem that requires at least 1k specified
residues. That's it. Have any examples?
> Sean is implicitly making an "irreducable
> complexity" argument here because he implies that for this useful
> feature to have come about it by evolution it must have come all in one
> go, because half a thumb is no good to a panda. He is also stating that
> the genetic difference between no false-thumb and having one is far too
> big to have occured in a single mutation, which is of course a
> straw-man because nobody has ever seriously proposed that.
>
> For us to accept Sean's argument, we would first have to accept Behe's
> irreducable complexity. This centeral dogma of modern day creationism
> has been widely debunked and has near zero acceptance outside of the ID
> / American fundamentalist community.
All functional systems are irreducible. The problem is that different
types of functions require different minimum structural threshold
requirements. As it turns out, the gaps between those functions that
have few minimum structral requirements are relatively small and easily
crossable via random mutation and function-based selection. However,
those functions with greater and greater minimum structural
requirements grow farther and farther away from the next closest
potentially beneficial genetic sequence within the potential of
sequence space. This increase in gap distance is linear in nature with
each increase in the minimum structural requirement. With each linear
increase in gap distance, the average number of mutations required to
achieve success increases exponentially.
> "High level functions" might be the combination of a very large number
> "low level functions", just like a long meandering walk could be called
> a combination of every single little step that took you closer to the
> point where you are right now. In order to accept this Behe position
> you would have to first believe that little changes cannot add up to
> big changes, or you would have to believe that a sequence of small
> changes which each have practical benefit cannot exist.
That's basically correct. Little changes do not add up to bigger and
bigger changes with respect to function as one moves up the ladder of
functional complexity. Bigger and bigger changes are required, on
average, to take each successive step up the ladder.
> The common rebuttals to Beheism is that co-option, the principle that a
> protien that has some apparant function in life today may have been
> used differently by the ancestor of that life-form. If you believe in
> Beheism you have to believe that cooption is non-existent or somehow
> irrelevant.
Not true. There are many real time examples of cooptation taking place
today. It is just that the odds for successful cooptation become
exponentially more and more remote as you move up the ladder of
functional complexity. All observable examples produce only low-level
biosystem functions with minimum structural threshold requirements of
less than a few hundred specified residues.
> The great thing is that even IDers have difficulty disputing the notion
> that genes which confer some kind of reproductive advantage are
> selected for by the environment.
IDers don't dispute this concept at all. Once a gene produces a
selective reproductive advantage, it will be selected or maintained, in
a positive way, by nature.
> If the population of genes are
> changing (via what Sean referrs to as Mendellian selection), and the
> content of these genes are changing via occasional mutation then you
> have every ingredient you need for the kind of very slow, gradual
> evolution that I am proposing.
Again, Mendelian "change" doesn't actually produce anything new within
the gene pool of options. You are still confused here. No functional
evolution happens during Mendelian variation. That is why Mendelian
variation would never produce a reptile from a fish, etc. In order to
do that, you need novel genetic codes coding for novel biosystem
functions. You need random mutations within existing gene pools.
Now, there are many examples of random mutations finding novel as well
as beneficial functional systems when those systems. However, such
examples never produce any type of novel function that requires a
minimum of more than a few hundred specifically arranged amino acid
residues working together at the same time. There's not a single
example of such a mechanism producing any novel function with a minimum
threshold requirement of more than 1,000 residues. Not one example in
all of literature. In fact, there is a clear stalling out effect as
one moves up the ladder toward this threshold limitation that is
exponential in nature.
Sean Pitman
www.DetectingDesign.com
ouroboros rex
<sea...@naturalselection.0catch.com> wrote in message
news:1167842594.5...@48g2000cwx.googlegroups.com...
>
> For my part, I've already shown you, over and over again, that gene
> duplications do not produce any novel function at all. They just
> produce more of the same thing. At this point, you need additional
> mutational modifications to achieve a novel function. The number of
> random modifications needed at higher levels of functional complexity,
> on average, would require trillions upon trillions of years.
Why? And even if true, wouldn't you have to divide by number of cases?
There are a lot of cells out there, doctor.
Seanpit
The calculations assume a population the size of all the bacteria on
Earth (about 1e30). Massive population sizes really don't solve the
problem - not even remotely close.
Sean Pitman
www.DetectingDesign.com
ouroboros rex
"Seanpit" <seanpi...@naturalselection.0catch.com> wrote in message
news:1167855036....@v33g2000cwv.googlegroups.com...
I'd be interested in seeing those.
Seanpit
Clyde Squid wrote:
> > The problem is that not all types of functions that are present within
> > biosystems are created equal. Different types of functions require
> > different minimum size and specificity structural requirements. Some
> > functions only require a few residues while others require many
> > specifically arranged residue structural "parts" in order for a
> > particular function to work - even a little bit.
>
> What functions are you talking about? What are "parts" in your world?
Protein-based functions, which require building blocks otherwise known
as amino acid residues.
> > Evolving low-level functions is kinda like finding a meaningful
> > 3-letter character sequence in the English language system. It is
> > fairly easy to do because the ratio of potentially
> > meaningful/beneficial vs. non-beneficial sequences is relatively high
> > (about 1 in 18 or so).
>
> Wow, look, numbers. Where did they come from?
How many defined 3-character sequences are there in the
English-language system? Of these, only a minority would be
theoretically "beneficial" given a certain situation/environment.
Given use of 26 letters plus a space character and a period (28
potential characters per position), the total number of potential
3-character sequences is 28^3 = a sequence space of 21,952 potential
options. Of these, only about 1000 or so are defined as "meaningful".
That produces a ration of about 1 in 22 meaningful vs. meaningless
sequences. Adding in a few two-word sequences produces a very generous
ratio (for your position) of 1 in 18 or so. Of those sequences that
are defined as "meaningful", only a few would be of any beneficial
meaning in a given situation/environment.
Even so, this ratio is relatively high compared to potentially
beneficial vs. non-beneficial 7-character sequences. The 7-character
sequence space is 28^7 = 13,492,928,512. Only about 23,000
seven-letter words are defined as meaningful in the English language
system. That produces a ratio of meaningless vs. potentially
meaningful of about 1 in 500,000. Given a certain degree of
flexibility and multiword 7-character sequences, the ratio may increase
to about 1 in 250,000 if one is very generous. However, when one
considers that the number of meaningful and potentially beneficial
7-character sequences is going to be much less than this ratio, one
starts to really understand the exponential nature of this problem.
The ratio decreases exponentially with each step up the minimum
structural threshold ladder of functional complexity.
> > However, this ratio drops exponentially when it
> > comes to finding higher and higher level functions. For example, the
> > ratio of potentially beneficial vs. non-beneficial 7-character
> > sequences drops to less than 1 in 250,000.
>
> I don't know where you are getting these numbers, but I strongly
> suspect that they are total crap. If you wish me to think otherwise,
> source please.
These numbers are the result of common sense. If you disagree, please
do explain how my numbers are significantly off here . . .
> > So, you see, it gets exponentially harder and harder to keep jumping up
> > to the next higher level of functions with greater minimum size and/or
> > specificity requirements.
>
> Not really. Look into developmental biology. Small changes in genes
> can result in very selectable differences in developmental patterns.
Almost always this is the result of a loss of a pre-established
function. Any time such mutational changes actually result in a gain
of a novel genetic biosystem function, that function has a relatively
low structural threshold requirement of less than a few hundred
specified residues. No novel function with minimum structural
threshold requirements of 1000aa or more has ever been shown to evolve
with either small or large genetic changes. It just doesn't happen.
> >This means that exponentially more and more
> > time is required to cross the gap between what is and what might be
> > beneficial at higher and higher functional levels. Very quickly
> > trillions upon trillions of years of time, on average, are required to
> > evolve any novel beneficial function at the next higher level.
>
> What peer-reviewed papers can I read that discuss this "gap" of yours
> in greater detail. I would love to read them. I don't see the math,
> and I doubt your numbers. Citation please.
Do your own calculations and see if I am not correct here. Go ahead;
Prove me wrong . . .
> > Consider that novel low level functions, those functions that require
> > less than 100 fairly specified residues, evolve on a fairly regular
> > basis in a wide variety of living organisms. However, those functions
> > that require at least 3 to 5 hundred residues are much more difficult
> > to evolve and are usually limited to a single type of organism with
> > specific features (like very fortuitous starting points). Now, note
> > that no functions that require at least 1000 specifically arranged
> > residues ever evolve. There isn't a single documented case in all of
> > scientific literature.
>
> I'm sorry, but this makes no sense. Your terminology is unclear, and I
> gather that's intentional. When you say residue, do you mean amino
> acid?
Is the term "residue" really that unclear to you? The term "amino
acid" really isn't the most correct term in this context. We are
talking about chains of amino acids that have been hooked together to
form a protein or collection of proteins. The term for amino acids in
such a chain is "residues".
> And what it is a "novel low level function.?"
Any biosystem function that requires less than 1000 specifically
arranged residues, at minimum, is what I would call a "low level"
function. For example, one can obtain a useful lactase function with
about 380aa, nylonase about 200aa, insulin about 50aa, etc. All of
these are low-level functions. In comparison, the function of
flagellar motility requires at least 10,000 fairly specifically
arranged residues.
> And this whole
> 1000 specifically arranged residues thing, I'm not buying it. I'm not
> saying I won't, it's just that you are not being in the least bit
> clear. Try again, this time with sources.
>
> > This observation of the stalling out of evolutionary potential is a
> > fact that is clearly documented. The obvious reason for this stalling
> > out effect is due to the exponential expansion of the non-beneficial
> > gap problem. The only means of getting across this gap is random
> > mutation. Natural selection is helpless because nature can only
> > select, in a positive way, those mutations that result in some
> > functional improvement over what came before. Stepping from an island
> > of beneficial function into the non-beneficial gap that exists between
> > high-level functions is a detrimental step, from the perspective of
> > natural selection. Therefore, nature will select to remove that
> > mutational sequence from the gene pool. Sometimes a sequence may be
> > allowed to undergo random walk for a while within the gap, but both
> > random walk and random mutational steps of any size have approximately
> > the same likelihood of finding a novel beneficial sequence within the
> > vast potential of sequence space (exponentially more vast with each
> > additional minimum size requirement).
>
> No one has observed evolution stalling out. You are now just stating
> that things can't happen based on nothing more than your own personal
> wishes. You have failed to make an argument for anything, as your
> words are unclear, your numbers unsubstantiated, and your conclusions
> therefore baseless. And you have yet to propose what did happen. Puff
> of smoke?
What did happen is obviously ID. ID is required as part of the origin
of those systems of function that have a minimum threshold of just a
few thousand specifically arranged residues. If you think this is puff
and smoke, show me an example of evolutionary mechanisms actually
producing any novel function beyond this minimum threshold level.
> When are you ID people going to stop trying to prove that evolution
> didn't do it and start getting around to providing evidence for what
> did happen? Positive evidences? Unqualified numbers used to show what
> you think didn't happen doesn't impress me or anybody else.
When are you going to figure out that the scientific method never
proves anything with absolute certainty? Hypotheses can only be
disproved absolutely. The ID hypothesis gains predictive value as long
as nothing comes along that disproves it. For example, I can never
fully prove that a cow cannot jump over my house this side of eternity,
but my hypothesis that this is impossible gains predictive value with
every failed cow-jump attempt. The same thing is true of the ID
hypothesis when it comes to genetic evolution. I'm hypothesizing that
the evolutionary mechanism will not be able to jump across the
non-beneficial gaps to achieve any novel function beyond a minimum
structural threshold of just 1000aa. This hypothesis is easily
falsifiable. All you need is just one example. Otherwise, this
hypothesis of mine gains more and more predictive value. That's how
science works.
> > In the end, jumping farther into the non-beneficial gap doesn't improve
> > the odds of success and evolutionary processes stall out completely on
> > very low rungs of the ladder.
>
> You have failed to show that such a gap exists, failed to provide any
> way for us to check your math, and failed to show you reached your
> conclusion by any means other than whispers from the gods. Please work
> on this.
Try thinking it through a bit more for yourself. See if you can counter
any of my proposed hypotheses . . . I'd be most interested and even
grateful if you succeed.
> Clyde
Sean Pitman
www.DetectingDesign.com
Seanpit
ouroboros rex wrote:
> >> > For my part, I've already shown you, over and over again, that gene
> >> > duplications do not produce any novel function at all. They just
> >> > produce more of the same thing. At this point, you need additional
> >> > mutational modifications to achieve a novel function. The number of
> >> > random modifications needed at higher levels of functional complexity,
> >> > on average, would require trillions upon trillions of years.
> >>
> >> Why? And even if true, wouldn't you have to divide by number of cases?
> >> There are a lot of cells out there, doctor.
> >
> > The calculations assume a population the size of all the bacteria on
> > Earth (about 1e30). Massive population sizes really don't solve the
> > problem - not even remotely close.
>
> I'd be interested in seeing those.
Go to: http://www.detectingdesign.com/flagellum.html
In the "Table of Contents", click on the link for "Trillions upon
Trillions of Years". Then, in the first paragraph, click on the link
for "calculation".
Sean Pitman
www.DetectingDesign.com
Seanpit
Did you even read the post? Are you only interested in what other
evolutionists have to say about your question? What about at least
hearing out a proposed answer to your valid question from a real
creationist?
Sean Pitman
www.DetectingDesign.com
CreateThis
<seanpi...@naturalselection.0catch.com> wrote:
Why? Listening to a "real creationist" is like wondering what the
Jehova's Witness on my doorstep wants. We already know the answer -
his lips are moving, so it must be "goddidit".
CT
Marc
sea...@naturalselection.0catch.com wrote:
> Marc wrote:
> > Marc wrote:
> > > Seanpit wrote:
> > > > Clyde Squid wrote:
> >
> > C'mon Sean - at least have a go at reading these and explaining why
> > they are not good enough for you to change your thinking.
>
> We've gone over this many times before Marc. These references you list,
> which you still haven't read yourself,
That's BULLSHIT, Sean - before I read anything else, I'll say that.
You have NO IDEA what I read or don't read - and ask Wilkins or
Don Cates if I actually have these papers, why don't you? And since
my access to them allows me to get them, why WOULDN'T I read them?
Whilst - and I've said this before, too - whilst at home when I cite
these I may only get to read the abstracts, my work PC uses
USYD as my ISP and so I can connect straight into their excellent
library e-journal collection. My boss is not real happy with the time
I do spend on the literature rather than numbering test tubes in the
lab, so I am at a bit of risk job-wise from reading these damn papers
to argue with you about them, so put your god-damn LIE about my
reading up your ass where the damn sun can never shine, dude.
Maybe *YOU* should read one or two of these rather than dismiss
them out-of-hand as you do every time. Answer this - why are there
eighty new papers in just a couple of months if they are all wrong?
> do nothing more than assume
> common decent via gene duplication and mutational divergence, etc.
That is also bullshit - you just don't want to admit anything about
this vast literature because IT KILLS YOUR GAP THEORY DEAD.
> None of these assumptions has ever been demonstrated when it comes to
> producing a novel function that requires more than 1,000 amino acid
> residues working together at the same time in a fairly specific 3D
> orientation with each other. No such level of functional complexity
> ever evolves.
Says he who won't read the abstracts let alone the papers. Can you GET
the papers Sean? Would you like me to post you a CD with a paper for
every residue you imagine can't evolve? (Ask Don how many papers are
on the copy od my backup CD from the 2005/2006 literature I gave him.)
> There's not a single documented case in all of
> literature.
EVERY PAPER I CITED shows such evidence (if you'd open your
eyes and/or mind). What do you think these papers are all about?
(Oh... "just-so stories", right? ..... You are being a Stupid Asshole.)
> Beyond this, none of your papers deal with the statistical
> likelihood of any higher level function evolving. The authors simply
> assume that it happened based soly on sequence comparisons and the
> assumption that similar sequences could only come about via
> evolutionary mechanisms of random mutation and function-based
> selection.
The way you expess terms in this passage shows how ingrained
your mistaken thinking is - it is like a bad mantra of evil ("similar
sequences could only come about via evolutionary mechanisms
of random mutation and function-based selection...") which you
utter without thought. Gene duplication leads to one process
of generation of new features, genome shuffling adds to that,
and complete genome duplication provides a DIFFERENT means
for evolution of new features since, amonst other things, it avoids
gene dosage problems that simple duplications run into. These
larger scale "mutations" are a major force in evolution and the
effect of selection is also something that you need to think
more about. (How can you understand selection when you deny
the major mutational events that give it something to act on?)
In the earlier list of papers there was one that explicitly proved
their point in a novel fashion - but in your wisdom they too must
be wrong, I guess. There is no reason to dismiss sequence data,
Sean, except that *ALL* the sequence data proves you wrong.
OH... Your "Immunity" page still REALLY SUCKS - plus it uses a
major falsehood to try to provide "logical" support for your twisted
ideas. I've half a mind to re-write your "improved" version for you
so you can at least get the basic Immunology somewhat right.
(signed) marc
.
Marc
................ snp....
> For my part, I've already shown you, over and over again, that gene
> duplications do not produce any novel function at all.
You have not *SHOWN* any such thing. You *have* declared it,
you have *assumed* it, you have cried it from mountain tops, but
you have *never* _shown_ it and you can't. You're wrong and you
have to LIE to "show" it.
Every paper I cited in the other reply in this thread, every paper
that was cited to you Nov. 21st and every paper cited months
before that *SHOWS* that duplication of genes or genomes leads
to new functions in the protein family concerned. Every report says
something about a different protein family or in a different species
and they all have the same theme (which you dismiss because
you don't like sequence data being studied).
> They just produce more of the same thing. At this point, you
need additional mutational modifications to achieve a novel function.
Just what do you think those papers (you *OBVIOUSLY* never read)
are all about? Hundreds upon hundreds of papers that all say, when
you read between the lines just a litle bit - "Sean Pitman Is Wrong".
> The number of
> random modifications needed at higher levels of functional complexity,
> on average, would require trillions upon trillions of years. That's
> the problem as I see it.
> If you disagree, by all means, prove me wrong.
The cited literature shows clearly you are wrong, the proof is there
and it is just getting you to *READ* the literature that is the hard
part.
> > Beside duplications of genes (which clearly lead to novel functions)
> > there are mechanisms for domain shuffling. What do these do, Sean?
>
> Please show me just one example were domain shuffling or gene
> duplications of any kind produced a novel function beyond mear
> assumption. It just doesn't happen Marc. There isn't such an example
> beyond very low levels of functional complexity.
I asked you once before, where do the major domains of the MHC
class II structure come from, Sean? Try that one as a result of
exon shuffling. (You get class I and II a bit confused on your web
page, so this may be a bit outside your grasp.)
(signed) marc
.
John Harshman
> sea...@naturalselection.0catch.com wrote:
>
>>Marc wrote:
>>
>>>Seanpit wrote:
>>>
>>>>Blodgett wrote:
>
>
> ................ snp....
>
>
>>For my part, I've already shown you, over and over again, that gene
>>duplications do not produce any novel function at all.
>
>
> You have not *SHOWN* any such thing. You *have* declared it,
> you have *assumed* it, you have cried it from mountain tops, but
> you have *never* _shown_ it and you can't. You're wrong and you
> have to LIE to "show" it.
>
> Every paper I cited in the other reply in this thread, every paper
> that was cited to you Nov. 21st and every paper cited months
> before that *SHOWS* that duplication of genes or genomes leads
> to new functions in the protein family concerned. Every report says
> something about a different protein family or in a different species
> and they all have the same theme (which you dismiss because
> you don't like sequence data being studied).
All this is inferred from gene or organismal phylogenies. Sean doesn't
believe in phylogenies. He's a creationist. And he thinks that his
personal disbelief allows him to reject the evidence out of hand.
What Sean is asking for is for a gene duplication to evolve into
multiple functions while he watches. Absence of such events falsifies
evolution (in his world, where the sky is a lovely shade of violet).
(Behe takes a similar position on ID; though he accepts common descent,
unlike Sean, he does demand that scientists grow flagellae on bacteria
while he watches.)
[snip]
Glenn
John Harshman wrote:
> Marc wrote:
>
> > sea...@naturalselection.0catch.com wrote:
> >
> >>Marc wrote:
> >>
> >>>Seanpit wrote:
> >>>
> >>>>Blodgett wrote:
> >
> >
> > ................ snp....
> >
> >
> >>For my part, I've already shown you, over and over again, that gene
> >>duplications do not produce any novel function at all.
> >
> >
> > You have not *SHOWN* any such thing. You *have* declared it,
> > you have *assumed* it, you have cried it from mountain tops, but
> > you have *never* _shown_ it and you can't. You're wrong and you
> > have to LIE to "show" it.
> >
> > Every paper I cited in the other reply in this thread, every paper
> > that was cited to you Nov. 21st and every paper cited months
> > before that *SHOWS* that duplication of genes or genomes leads
> > to new functions in the protein family concerned. Every report says
> > something about a different protein family or in a different species
> > and they all have the same theme (which you dismiss because
> > you don't like sequence data being studied).
>
> All this is inferred from gene or organismal phylogenies. Sean doesn't
> believe in phylogenies. He's a creationist. And he thinks that his
> personal disbelief allows him to reject the evidence out of hand.
I thought you believed inferences do "demonstrate" or "show".
>
> What Sean is asking for is for a gene duplication to evolve into
> multiple functions while he watches. Absence of such events falsifies
> evolution (in his world, where the sky is a lovely shade of violet).
I don't recall Sean ever claiming he needed to see something happen
"while he watches". Many observations take more time than we normally
associate with what you intimate.
But an absense of observations as a result of failure to demonstrate,
evidence of the ability of genetic changes to produce novel functions
would seem quite sufficient to falsify theory.
Can you provide a reference of an observation of a pseudogene acquiring
a new function?
I understand there are a lot of them in "junk dna".
>
> (Behe takes a similar position on ID; though he accepts common descent,
> unlike Sean, he does demand that scientists grow flagellae on bacteria
> while he watches.)
>
Well I don't see the problem. Maybe my understanding of Sean's position
is incorrect, but it appears to me that disproof would be easy to
demonstrate; any change to a gene or sequence that produces a protein
consisting of over 1000 amino acids resulting in a different (novel)
function.
Marc
Looking at the "gene duplication" literature yesterday,
I noticed this very recent report ... it's not available in
free, full text but if you ask nicely somebody might
forward the pdf to you. (The abstract is fairly clear, anyway.)
"Frequent emergence and functional resurrection of processed
pseudogenes in the human and mouse genomes."
Gene. 2006 Nov 18; [Epub ahead of print] PMID: 17196768
by Sakai and others.
Abstract: Despite the wide distribution of processed pseudogenes
in mammalian genomes, such as those of human and mouse,
relatively little is known about their roles in genomic evolution.
While gene duplications are recognized as one of the major
driving forces in genome evolution, processed pseudogenes,
which are retrotransposed copies of mRNAs, have been regarded
as junk or selfish DNA for a long time. In order to elucidate the
quantitative and qualitative contribution of processed pseudogenes
to the mammalian genome evolution, we attempted to detect
processed pseudogenes by extensively mapping the mRNAs
to both the human and mouse genomes, and then we estimated
the rate of their emergence. As a result, we revealed that the rate
of pseudogene emergence was about 1-2% per gene per million
years, which was as high as the rate (0.9%) of gene duplication
in the human genome, although the rate of pseudogene emergence
was found to drastically decrease in the hominid lineage. Furthermore,
1% of the processed pseudogenes seemed to be reinvigorated by
post-retrotransposition transcription, many of them preserving the
intact coding regions. Since the expression patterns of transcribed
pseudogenes in various tissues were quite different between human
and mouse, their emergence might have led to species-specific
evolution. Our results indicate that the generation of processed
pseudogenes was not wholly futile but instead has been an
indispensable resource, driving dynamic evolution of the mammalian
genomes.
> I understand there are a lot of them in "junk dna".
> >
> > (Behe takes a similar position on ID; though he accepts common descent,
> > unlike Sean, he does demand that scientists grow flagellae on bacteria
> > while he watches.)
> >
> Well I don't see the problem. Maybe my understanding of Sean's position
> is incorrect, but it appears to me that disproof would be easy to
> demonstrate; any change to a gene or sequence that produces a protein
> consisting of over 1000 amino acids resulting in a different (novel)
> function.
Sean rejects the research out-of-hand if it involves sequence data.
> "None of these assumptions has ever been demonstrated when it comes to
> producing a novel function that requires more than 1,000 amino acid
> residues working together at the same time in a fairly specific 3D
> orientation with each other. No such level of functional complexity
> ever evolves."
It does all the time - read the duplication literature cited in this
thread
yesterday, elsewhere on Nov. 21st and again before that. Sean just
says "it's a bunch of just-so stories" when it is actually very serious
research accepted widely in the biological science community.
(signed) marc
.
John Harshman
That's right. Problem?
>>What Sean is asking for is for a gene duplication to evolve into
>>multiple functions while he watches. Absence of such events falsifies
>>evolution (in his world, where the sky is a lovely shade of violet).
>
> I don't recall Sean ever claiming he needed to see something happen
> "while he watches". Many observations take more time than we normally
> associate with what you intimate.
> But an absense of observations as a result of failure to demonstrate,
> evidence of the ability of genetic changes to produce novel functions
> would seem quite sufficient to falsify theory.
You will have to put that into clear English.
> Can you provide a reference of an observation of a pseudogene acquiring
> a new function?
> I understand there are a lot of them in "junk dna".
There are such examples, but they all depend on phylogenetic analysis.
>>(Behe takes a similar position on ID; though he accepts common descent,
>>unlike Sean, he does demand that scientists grow flagellae on bacteria
>>while he watches.)
>
> Well I don't see the problem. Maybe my understanding of Sean's position
> is incorrect, but it appears to me that disproof would be easy to
> demonstrate; any change to a gene or sequence that produces a protein
> consisting of over 1000 amino acids resulting in a different (novel)
> function.
>
> "None of these assumptions has ever been demonstrated when it comes to
> producing a novel function that requires more than 1,000 amino acid
> residues working together at the same time in a fairly specific 3D
> orientation with each other. No such level of functional complexity
> ever evolves."
Define "different". How different does the function have to be? And does
it have to happen while we watch? If not, how do we determine that it's
a change, rather than something that was always there? (I know how I
determine that: again, through phylogenetic analysis.)
John Harshman
No, he rejects it out of hand if it involves any kind of inference about
the past. In the case of the processed pseudogenes, he would reject the
idea that they were retroviral insertions or that they had ever been
non-functional, or any different than they are now seen to be. It's only
by chance (or some mysterous plan of the creator) that they resemble
reverse-transcribed, processed mRNAs.
>>"None of these assumptions has ever been demonstrated when it comes to
>>producing a novel function that requires more than 1,000 amino acid
>>residues working together at the same time in a fairly specific 3D
>>orientation with each other. No such level of functional complexity
>>ever evolves."
>
> It does all the time - read the duplication literature cited in this
> thread
> yesterday, elsewhere on Nov. 21st and again before that. Sean just
> says "it's a bunch of just-so stories" when it is actually very serious
> research accepted widely in the biological science community.
Like I said, it's because he rejects all conclusions that are based on
phylogenetic analysis. He doesn't believe in phylogeny, so he gets to
ignore it.
calebw...@gmail.com
short period of time.... i mean the world has been around for billions
of years and something like the evolution of birds did not happen in a
year or so it happend over millions of years threw the process of
natural selection...also anyone that tries to argue that natural
selection does not support evolution is ignorant........ An example of
micro evolution is the finches on galapagos island... but the evolution
of the bird it self was a much longer process.... look up the way birds
came around... the therapod dinosaur... it shows how a process of
diffrent micro evolutions in short periods of time on the dinosaur
ended up becoming a whole new species showing macro evolution... there
both the same thing its just the amount of time both happen in and the
variance of evolution to the creature.
JTEM
Seanpit wrote:
> JTEM wrote:
> > Seanpit wrote:
> > > The analogy really isn't so bad. It's pretty good
> > > actually.
> >
> > ....NOT!
>
> Did you even read the post?
I got about two paragraphs past the opening insanity
before giving up.
> Are you only interested in what other evolutionists
> have to say about your question?
Nope. But I'd rather get no I.D.iots to respond than the
loose collection of misrepresentations & false tests
that you provided.
> What about at least hearing out a proposed answer
> to your valid question from a real creationist?
There was nothing valid in the nonsense I was responding
to. Nothing.
Seanpit
Marc wrote:
> sea...@naturalselection.0catch.com wrote:
> > Marc wrote:
> > > Marc wrote:
> > > > Seanpit wrote:
> > > > > Clyde Squid wrote:
> > >
> > > C'mon Sean - at least have a go at reading these and explaining why
> > > they are not good enough for you to change your thinking.
> >
> > We've gone over this many times before Marc. These references you list,
> > which you still haven't read yourself,
>
> That's BULLSHIT, Sean - before I read anything else, I'll say that.
>
> You have NO IDEA what I read or don't read
You have history of not reading what you reference - of blind
referencing (which is even worse than quote mining). Given that
consistent history, the predictive value of the hypothesis that you
will maintain such behavior is quite good.
> - and ask Wilkins or
> Don Cates if I actually have these papers, why don't you? And since
> my access to them allows me to get them, why WOULDN'T I read them?
>
> Whilst - and I've said this before, too - whilst at home when I cite
> these I may only get to read the abstracts, my work PC uses
> USYD as my ISP and so I can connect straight into their excellent
> library e-journal collection. My boss is not real happy with the time
> I do spend on the literature rather than numbering test tubes in the
> lab, so I am at a bit of risk job-wise from reading these damn papers
> to argue with you about them, so put your god-damn LIE about my
> reading up your ass where the damn sun can never shine, dude.
> Maybe *YOU* should read one or two of these rather than dismiss
> them out-of-hand as you do every time. Answer this - why are there
> eighty new papers in just a couple of months if they are all wrong?
They all make the same assumption. It's just that this assumption is
not the only potentially valid explanation. And, this common
assumption is not backed up by any demonstration whatsoever beyond the
1000aa level.
> > do nothing more than assume
> > common decent via gene duplication and mutational divergence, etc.
>
> That is also bullshit - you just don't want to admit anything about
> this vast literature because IT KILLS YOUR GAP THEORY DEAD.
Even some of the references that you yourself have provided for me
actually admit that this assumption is just that - an assumption.
Again, list just one reference that actually demonstrates this
assumption beyond the 1000aa level. There are lots of examples below
this level, but not one beyond this level. Interesting - don't you
think? What might be the explanation for this interesting phenomenon?
> > None of these assumptions has ever been demonstrated when it comes to
> > producing a novel function that requires more than 1,000 amino acid
> > residues working together at the same time in a fairly specific 3D
> > orientation with each other. No such level of functional complexity
> > ever evolves.
>
> Says he who won't read the abstracts let alone the papers. Can you GET
> the papers Sean? Would you like me to post you a CD with a paper for
> every residue you imagine can't evolve? (Ask Don how many papers are
> on the copy od my backup CD from the 2005/2006 literature I gave him.)
I only want one paper, just one, that actually demonstrates the
evolution of a novel functional molecular biosystem beyond the 1000aa
level. I don't want sequence based assumptions here. I want a
demonstration or, at the very least, some sort of statistical analysis
dealing with the proposed evolutionary mechanism and the odds or
average time needed to achieve said function. As far as I am aware,
there are no such papers in all of scientific literature. Not a single
one. All of the ones you reference base everything on the *assumption*
of common decent because of sequence similarities - not demonstration
or relevant statistical analysis with regard to mechanism.
> > There's not a single documented case in all of
> > literature.
>
> EVERY PAPER I CITED shows such evidence (if you'd open your
> eyes and/or mind). What do you think these papers are all about?
> (Oh... "just-so stories", right? ..... You are being a Stupid Asshole.)
That's right! Just-so stories without any demonstration or relevant
statistical analysis with regard to mechanism. Everything behind the
conclusions of these authors you cite is based on the assumption that
sequence similarities can only be achieved via evolutionary
relationships. This assumption has yet to be supported by actual
falsifiable empirical or statistical testing with regard to the
proposed mechanism.
> > Beyond this, none of your papers deal with the statistical
> > likelihood of any higher level function evolving. The authors simply
> > assume that it happened based soly on sequence comparisons and the
> > assumption that similar sequences could only come about via
> > evolutionary mechanisms of random mutation and function-based
> > selection.
>
> The way you expess terms in this passage shows how ingrained
> your mistaken thinking is - it is like a bad mantra of evil ("similar
> sequences could only come about via evolutionary mechanisms
> of random mutation and function-based selection...") which you
> utter without thought. Gene duplication leads to one process
> of generation of new features, genome shuffling adds to that,
> and complete genome duplication provides a DIFFERENT means
> for evolution of new features since, amonst other things, it avoids
> gene dosage problems that simple duplications run into. These
> larger scale "mutations" are a major force in evolution and the
> effect of selection is also something that you need to think
> more about. (How can you understand selection when you deny
> the major mutational events that give it something to act on?)
I don't deny these types of mutational events at all. Where did you
get that? I think it perfectly possible and even likely that
duplication events, like the ones you describe, can and do occur (many
have actually been demonstrated on a regular basis). I just don't
think these mutations produce any novel genetic functions beyond the
1000aa threshold. Go ahead and prove me wrong. Show me were any type
of mutation has ever been demonstrated to cross this threshold in real
life or via relevant statistical analysis with regard to mechanism.
> In the earlier list of papers there was one that explicitly proved
> their point in a novel fashion - but in your wisdom they too must
> be wrong, I guess. There is no reason to dismiss sequence data,
> Sean, except that *ALL* the sequence data proves you wrong.
Sequence data doesn't "prove" mechanism Marc. How can you not see
that? The mechanism behind the sequence data is simply assumed without
actual demonstration when it comes to actually producing novel
functional systems beyond the 1000aa level.
> OH... Your "Immunity" page still REALLY SUCKS - plus it uses a
> major falsehood to try to provide "logical" support for your twisted
> ideas. I've half a mind to re-write your "improved" version for you
> so you can at least get the basic Immunology somewhat right.
LOL - Given your history of misunderstanding how the immune system and
other such evolving systems relate to real evolutionary processes, I'd
hold back if I were you . . .
Seanpit
Come on now, can you explain why there is a stalling out effect of
evolutionary mechanisms with functions that have greater and minimum
structral threshold requirements? This observation is a fact clearly
evident in scientific literature. What's your explanation for this
very real observation?
Sean Pitman
www.DetectingDesign.com
Seanpit
> > Marc wrote:
> John Harshman wrote:
> >>For my part, I've already shown you, over and over again, that gene
> >>duplications do not produce any novel function at all.
> >
> > You have not *SHOWN* any such thing. You *have* declared it,
> > you have *assumed* it, you have cried it from mountain tops, but
> > you have *never* _shown_ it and you can't. You're wrong and you
> > have to LIE to "show" it.
I've shown you the statistical reasons why your assumption of
evolutionary mechanisms doing what you think they did just isn't
tenable this side of trillions upon trillions of years of time. You
have yet to counter with any relevant statistical analysis of your own
with regard to the potential of your proposed mechanism. You simply
assume that your mechanism did the job in relatively short order
without any statistical backing whatsoever with regard to the workings
of your actual mechanism.
> > Every paper I cited in the other reply in this thread, every paper
> > that was cited to you Nov. 21st and every paper cited months
> > before that *SHOWS* that duplication of genes or genomes leads
> > to new functions in the protein family concerned. Every report says
> > something about a different protein family or in a different species
> > and they all have the same theme (which you dismiss because
> > you don't like sequence data being studied).
>
> All this is inferred from gene or organismal phylogenies. Sean doesn't
> believe in phylogenies. He's a creationist. And he thinks that his
> personal disbelief allows him to reject the evidence out of hand.
>
> What Sean is asking for is for a gene duplication to evolve into
> multiple functions while he watches. Absence of such events falsifies
> evolution (in his world, where the sky is a lovely shade of violet).
>
> (Behe takes a similar position on ID; though he accepts common descent,
> unlike Sean, he does demand that scientists grow flagellae on bacteria
> while he watches.)
I've said many times before that the demonstration of just a single
proposed step (beyond the 1000aa threshold) in the evolution of a
function as complex as flagellar motility would be enough to falsify my
position. What is most interesting here is that functions with lower
structural threshold requirements evolve all the time. Why is it then
that functions with a few more structural threshold requirements, only
1000aa, do not evolve in real time at all? Very simple functions do
evolve with those with a bit more complexity do not evolve with a
spectrum of the stalling-out effect in between. What's your
explanation? I mean really, if the individual steps are not separated
by sizable gaps, non-beneficial gaps that are significantly wider than
they are at lower levels, what is it that prevents a flagellar motility
system from evolving right before our eyes?
Sean Pitman
www.DetectingDesign.com
Ye Old One
<seanpi...@naturalselection.0catch.com> enriched this group when
s/he wrote:
>> >> Sean Pitman wrote:
>> > Marc wrote:
>> John Harshman wrote:
>
>> >>For my part, I've already shown you, over and over again, that gene
>> >>duplications do not produce any novel function at all.
>> >
>> > You have not *SHOWN* any such thing. You *have* declared it,
>> > you have *assumed* it, you have cried it from mountain tops, but
>> > you have *never* _shown_ it and you can't. You're wrong and you
>> > have to LIE to "show" it.
>
>I've shown you the statistical reasons why your assumption of
>evolutionary mechanisms doing what you think they did just isn't
>tenable this side of trillions upon trillions of years of time.
The problem is, for you, that evolution has occured to produce the
life we see all around us today. This proves you numbers are wrong.
[snip]
--
Bob.
John Harshman
>>>>Sean Pitman wrote:
>>>
>>>Marc wrote:
>>
>>John Harshman wrote:
>
>
>>>>For my part, I've already shown you, over and over again, that gene
>>>>duplications do not produce any novel function at all.
>>>
>>>You have not *SHOWN* any such thing. You *have* declared it,
>>>you have *assumed* it, you have cried it from mountain tops, but
>>>you have *never* _shown_ it and you can't. You're wrong and you
>>>have to LIE to "show" it.
>
> I've shown you the statistical reasons why your assumption of
> evolutionary mechanisms doing what you think they did just isn't
> tenable this side of trillions upon trillions of years of time. You
> have yet to counter with any relevant statistical analysis of your own
> with regard to the potential of your proposed mechanism. You simply
> assume that your mechanism did the job in relatively short order
> without any statistical backing whatsoever with regard to the workings
> of your actual mechanism.
No, he shows that the job was done. I don't think we've arrived at the
question of mechanism yet. First we have to establish that such things
have happened in the history of life, which the evidence does establish.
And it's clear that gene duplication has been an important part of that
process. Until we can agree on basics like that, we can't even begin to
address mechanism, because you will reject all the relevant evidence.
I predict that once again you will ignore questions of phylogeny in
favor of reiterating your "neutral gap" claims.
I predict also that you will ignore the independence of common descent
and intelligent design, claiming by elision that your neutral gap theory
falsifies common descent.
>>>Every paper I cited in the other reply in this thread, every paper
>>>that was cited to you Nov. 21st and every paper cited months
>>>before that *SHOWS* that duplication of genes or genomes leads
>>>to new functions in the protein family concerned. Every report says
>>>something about a different protein family or in a different species
>>>and they all have the same theme (which you dismiss because
>>>you don't like sequence data being studied).
>>
>>All this is inferred from gene or organismal phylogenies. Sean doesn't
>>believe in phylogenies. He's a creationist. And he thinks that his
>>personal disbelief allows him to reject the evidence out of hand.
>>
>>What Sean is asking for is for a gene duplication to evolve into
>>multiple functions while he watches. Absence of such events falsifies
>>evolution (in his world, where the sky is a lovely shade of violet).
>>
>>(Behe takes a similar position on ID; though he accepts common descent,
>>unlike Sean, he does demand that scientists grow flagellae on bacteria
>>while he watches.)
>
>
> I've said many times before that the demonstration of just a single
> proposed step (beyond the 1000aa threshold) in the evolution of a
> function as complex as flagellar motility would be enough to falsify my
> position. What is most interesting here is that functions with lower
> structural threshold requirements evolve all the time. Why is it then
> that functions with a few more structural threshold requirements, only
> 1000aa, do not evolve in real time at all?
Because you're making up a criterion that nobody else can figure out?
> Very simple functions do
> evolve with those with a bit more complexity do not evolve with a
> spectrum of the stalling-out effect in between. What's your
> explanation?
You made it up?
> I mean really, if the individual steps are not separated
> by sizable gaps, non-beneficial gaps that are significantly wider than
> they are at lower levels, what is it that prevents a flagellar motility
> system from evolving right before our eyes?
The question is meaningless. It turns all the complexity of evolution
into a ridiculously simple model with invented parameters.
But you are distracting attention from the point here, which is that you
refuse to accept the evidence of past evolution. On what basis?
John Harshman
Actually, that's not true. It merely proves that even if his claims are
correct they don't prevent evolution. What that would mean is that there
must be some additional mechanism other than random mutation and
selection operating to produce new adaptive structures. It could, for
example, be God providing a helpful hand across the odd neutral gap.
(If his claims are correct, that is. I don't think they are. But the
issues are separate.)
Seanpit
Ye Old One wrote:
> The problem is, for you, that evolution has occured to produce the
> life we see all around us today. This proves you numbers are wrong.
Really? If evolution is responsible for all that we see around us,
what mechanism was used to produce such diversity of form and function?
Where are your numbers to back up the creative potential of such a
mechanism?
> Bob.
Sean Pitman
www.DetectingDesign.com
ouroboros rex
I'm afraid that page is worthless, for too many reasons to go into here -
opaque writing, unexplained assumptions, bad case limitations, etc., etc.
Do you have a real cite?.
ouroboros rex
>
>
> The ratio decreases exponentially with each step up the minimum
> structural threshold ladder of functional complexity.
Google appears to find no evidence for the existence of this concept other
than your own writings, what else do you have? Not being a scientist or MD,
my search options are somewhat limited.
Is this why your 'calculations' page has those initial constrictions, like
1000 residues and such?
Just at a guess, it looks like you are claiming that the more advanced a
system was, the more genetic change would be required for the same type of
novel function...? I can't seem to make this follow, can you condense this
better for me?
Seanpit
ouroboros rex wrote:
> > The ratio decreases exponentially with each step up the minimum
> > structural threshold ladder of functional complexity.
>
> Google appears to find no evidence for the existence of this concept other
> than your own writings, what else do you have? Not being a scientist or MD,
> my search options are somewhat limited.
I don't know of anyone else presenting this concept either. However,
it isn't a difficult concept. The evidence for it is clearly evident.
As with any language or system of symbolic information coding and
transmission, genetically based biosystems are not created equal.
Different types of systems require different minimum numbers of parts
to be in a rather specific orientation with each other at the same
time. The greater the minimum threshold requirement, the exponentially
greater the size of the potential of sequence space.
So far, all of this is intuitively obvious. What is only slightly less
obvious is the fact that the ratio of potentially beneficial sequences
at a given level of minimum threshold requirements also drops in an
exponential manner relative to the ratio that exists at lower levels.
This is true of all information systems to include languages such as
English, computer code, genetics, etc.
> Is this why your 'calculations' page has those initial constrictions, like
> 1000 residues and such?
>
> Just at a guess, it looks like you are claiming that the more advanced a
> system was, the more genetic change would be required for the same type of
> novel function...? I can't seem to make this follow, can you condense this
> better for me?
That's right. In order to achieve a novel beneficial function in a
case where only a few specifically arranged structural basic structural
components are required (as in 3-letter sequences or 10 residue
proteins, etc), the average number of random mutations (of any kind)
needed to achieve success is relatively few. However, those functions
with additional threshold requirements require exponentially more
mutations, on average, before any one of them can be found. As the
number of threshold requirements increases linearly, the number of
mutational steps needed, on average, increases exponentially.
In order for a population to keep up, producing novel beneficial
functional systems of at greater and greater levels of threshold
requirements, the population size would also have to increase
exponentially (as you originally pointed out). The problem here is
that there are environmental constraints as well as other problems with
keeping such population expansion up for very long. Relatively
quickly, the maximum steady-state population and mutation rate cannot
maintain the same rate of evolution at higher threshold levels of
functionality and evolutionary mechanisms stall out, in an exponential
manner, with consideration of each higher level of functional threshold
limitations.
Sean Pitman
www.DetectingDesign.com
bullpup
>
> Ye Old One wrote:
>
> > The problem is, for you, that evolution has occured to produce the
> > life we see all around us today. This proves you numbers are wrong.
>
> Really? If evolution is responsible for all that we see around us,
> what mechanism was used to produce such diversity of form and function?
Natural Selection of variations. But you already know that
> Where are your numbers to back up the creative potential of such a
> mechanism?
Who needs numbers when the planet is literally crawling with directly
observed examples?
Boikat
Marc
...... snip
> You have history of not reading what you reference
I have a history of reading abstracts when I post from home and
then reading my post from work to get the papers themselves. They
then get read along with the other papers I collect that have nothing
to do with the posts here. At least I do eventually read the papers.
Your comment about my "not reading" is just a lie, Sean.
Also, what difference does it make if the paper was read by me?
These papers are the published scientific peer-reviewed primary
literature and what matters is not my reading them but your ignoring
them, so don't blow them off because of your lie about my interest
in the literature. What a lame excuse, Sean.
> - of blind
> referencing (which is even worse than quote mining). Given that
> consistent history, the predictive value of the hypothesis that you
> will maintain such behavior is quite good.
.... snip....
> > OH... Your "Immunity" page still REALLY SUCKS - plus it uses a
> > major falsehood to try to provide "logical" support for your twisted
> > ideas. I've half a mind to re-write your "improved" version for you
> > so you can at least get the basic Immunology somewhat right.
>
> LOL - Given your history of misunderstanding how the immune system and
> other such evolving systems relate to real evolutionary processes, I'd
> hold back if I were you . . .
Wait a minute here.
Your "evolutionary" process of B-cells undergoing somatic
hypermutation is actually more a stage of development than
it is a process of evolution. Over the course of evolution of
the vertebrate adaptive immunity the specfic mechanism
of hypermutation developed with specific enzymes that
target only certain regions of the antibody binding pocket.
Yes, there is "selection" of some cells over others so concepts
of evolution can apply, but to call this process the same as
mainstream "random mutation evolution of the species" is
bogus and to use a supposed failing of somation hypermutation
to perform as real evolution is a false argument (a "lie", dude)
as you use it on your site.
Please tell my why the explicit term is "SOMATIC hypermutation",
and why that extremely fast mutation rate is *not* the rate cited
as the mutation rate for evolution outside of B-cell CDR3 regions.
When cells undergo planned processes within the body that use
specific enzymes to make changes in just certain sites, and when
this process does not contribute to future generations or even build
on itself (somatic hypermutation only happens at very specific and
limited stages in a B-cell's life, and it does not go on and on), it is
more a process of developmental biology than it is evolutionary
biology. I have accepted that tumours which beging to be passed
between members of a species (as in dogsa and tassie devils) are
across the threshold of becoming an entity that is "evolving", so
you should learn to accept when you are wrong, too.
Another point - you make one of your "trillions of" type arguments
on your immunity page about the combinational diversity of the
antibodies but the problem is your calculations concern the
framework of the molecule and not the binding site. That is,
you use the "large numbers" argument as if that large diversity
was in fact in the antigen binding pockets, which it is not. Binding
sites are what is important but you ignore them and you also
ignore the limits of specificity by not allowing for any degree
of cross-reactivity or mimicry in antigen recognition. If you have
false arguments to base your conclusions on, what does that
say about your conclusions, "doctor"?
(signed) marc
.
Ye Old One
What numbers? It is not a matter of numbers.
The fact is that about 4 billion years ago life started on Earth. From
then to now we have a process called evolution that has, in response
to the environmental pressures, produced the diversity of life we see
around us today.
You can't put numbers to evolution, it is not a number based process.
--
Bob.
JTEM
Seanpit wrote:
> Come on now, can you explain why there is [...]
I couldn't hope to explain anything without specific
examples, but I can point out the fact that there is
no need to.
25 years ago we couldn't "Explain" how people got
AIDS. There were some who suspected a virus, even
some who believed it was sexually transmitted, but
nobody really knew.
Nobody entertained the notion of fairy dust or UFOs.
Get it? Even just a little? Even though not one single
person knew what was causing AIDS, or how it was
spread, nobody suggested that it must have been
magic or space aliens.
nickm...@gmail.com
Seanpit wrote:
> > And what it is a "novel low level function.?"
>
> Any biosystem function that requires less than 1000 specifically
> arranged residues, at minimum, is what I would call a "low level"
> function. For example, one can obtain a useful lactase function with
> about 380aa, nylonase about 200aa, insulin about 50aa, etc. All of
> these are low-level functions. In comparison, the function of
> flagellar motility requires at least 10,000 fairly specifically
> arranged residues.
Sean agrees that all of this can evolve, but he thinks it is utterly
impossible that a 380 aa protein might evolve to cooperate with another
similar size protein, and that this might happen a twice, producing a
system using over 1000 "specifically arranged" residues.
In other words, Sean thinks:
1 protein: possible
2 proteins (under 1,000 aas): possible
3 proteins (over 1,000 aas): absolutely impossible and therefore
evidence of divine intervention.
Another way of saying it.
1+1 = 2 -- Sean agrees
2+1 = 3 -- Sean disagrees
nickm...@gmail.com
Seanpit wrote:
> I only want one paper, just one, that actually demonstrates the
> evolution of a novel functional molecular biosystem beyond the 1000aa
> level. I don't want sequence based assumptions here. I want a
> demonstration or, at the very least, some sort of statistical analysis
> dealing with the proposed evolutionary mechanism and the odds or
> average time needed to achieve said function. As far as I am aware,
> there are no such papers in all of scientific literature. Not a single
> one. All of the ones you reference base everything on the *assumption*
> of common decent because of sequence similarities - not demonstration
> or relevant statistical analysis with regard to mechanism.
Here's a pathway with five or six required proteins that evolved in the
last 50 years or so:
Glenn R. Johnson, Rakesh K. Jain, and Jim C. Spain (2002). "Origins of
the 2,4-Dinitrotoluene Pathway." Journal of Bacteriology, August 2002,
p. 4219-4232, Vol. 184, No. 15.
http://www.doi.org/10.1128/JB.184.15.4219-4232.2002
nickm...@gmail.com
sea...@naturalselection.0catch.com wrote:
> It is just that the odds for successful cooptation become
> exponentially more and more remote as you move up the ladder of
> functional complexity.
Wild, undocumented, and clueless assertion. Bird wings are pretty
freaking complex, yet they have changed function multiple times in
various birds into flippers (penguins, flightless cormorant, giant auk,
etc.)
Nick
Seanpit
Ah yes, the 2,4-DNT pathway. I've discussed it several times in this
forum. While real, it isn't at a significantly higher level minimum
specified part requirements than is it's most complex single protein
part. Why not? Because it is a cascading function. As a cascade, it
doesn't require that all its parts be specifically arranged or oriented
relative to all the other parts at the same time (as is the case for
multiprotein functions like flagellar motility etc). Statistically
then, it is much much easier to obtain all the needed parts for a
cascading system than it is for a system of equivalent size that
additionally requires specific part orientation of all the parts at the
same time relative to each other.
In short, you have the size requirement here, but not the specificity
requirement.
Sean Pitman
www.DetectingDesign.com
P.S. You wouldn't be the same Nick Matzke who wrote the essay on
flagellar evolution would you? "Evolution in (Brownian) space: a model
for the origin of the bacterial flagellum"?
Seanpit
This is correct; except for the part about divine intervention. Any
high-level intelligence could produce the same type of creation. It
doesn't have to be the result of divine intelligence, just deliberate
intelligent activity of some kind that goes far beyond the realm of
what random mutation and function-based selection can achieve.
> Another way of saying it.
>
> 1+1 = 2 -- Sean agrees
> 2+1 = 3 -- Sean disagrees
2+1 always equals 3 - once it happens that 2 actually gets added to 1.
Sean Pitman
www.DetectingDesign.com
Seanpit
Are you arguing that the process of intelligent design is "magic"?
What about your own creative abilities? Are they "magical"? If you
can't remotely explain how your mindless mechanism can do the job, then
you have to at least consider the possibility that IDists just might
have something - that there just might be significant limitations
behind your proposed mechanism.
You asked where the "limitation" was for evolutionary mechanisms. I've
pointed a major one out to you and the best you have is "We know it
can't be a true limitation even if we don't yet know why."?! LOL - Now
that's science for you! ; )
Sean Pitman
www.DetectingDesign.com
Seanpit
All truly scientific hypotheses are based on predictive value, which is
a numbers based value. If you can't evaluate the abilities of your
proposed mechanism, statistically, how can you say that this mechanism
is more or less likely than any other potential mechanism? Hmmmmm?
You need numbers my man. Where are they?
> Bob.
Sean Pitman
www.DetectingDesign.com
Seanpit
Hmmmmm. You have a point. The problem is that these directly observed
examples never go beyond the 1000aa threshold of specifically arranged
residues. All of the examples out there are significantly lower-level
than 1000aa. Now why is that? What is it that prevents there being
any examples beyond this level? What is the statistical reason for
this phenomenon?
> Boikat
Sean Pitman
www.DetectingDesign.com
Seanpit
ouroboros rex wrote:
> >> >> There are a lot of cells out there, doctor.
> >> >
> >> > The calculations assume a population the size of all the bacteria on
> >> > Earth (about 1e30). Massive population sizes really don't solve the
> >> > problem - not even remotely close.
> >>
> >> I'd be interested in seeing those.
> >
> > Go to: http://www.detectingdesign.com/flagellum.html
> >
> > In the "Table of Contents", click on the link for "Trillions upon
> > Trillions of Years". Then, in the first paragraph, click on the link
> > for "calculation".
> >
> > Sean Pitman
> > www.DetectingDesign.com
>
> I'm afraid that page is worthless, for too many reasons to go into here -
> opaque writing, unexplained assumptions, bad case limitations, etc., etc.
Did you actually read the entire essay? If so, what unexplained
assumptions and limitations, specifically, need additional help?
> Do you have a real cite?
As far as I am aware, no one else is presenting this particular view.
Sean Pitman
www.DetectingDesign.com
Seanpit
So, the minimum size and complexity for the directed beneficial
swimming function requires a fairly sizable degree of part and
specificity requirements? Is that what you are trying to say?
Come on now Nick. Show many any molecular system where all the parts
work together at the same time beyond a minimum threshold level of 1000
specifically arranged residues evolving in real time. Your bird
example isn't one of them because the threshold requirements a minimum
selectable abilities were already in place ahead of time.
> Nick
Sean Pitman
www.DetectingDesign.com
Ye Old One
Life exists, in great diversity. All that life has evolved from
earlier life over the last 4 billion years. Where do you see the need
for numbers in that?
--
Bob.
bullpup
>
> bullpup wrote:
> > "Seanpit" <seanpi...@naturalselection.0catch.com> wrote in message
> > news:1167944850.3...@i15g2000cwa.googlegroups.com...
> > >
> > > Ye Old One wrote:
> > >
> > > > The problem is, for you, that evolution has occured to produce the
> > > > life we see all around us today. This proves you numbers are wrong.
> > >
> > > Really? If evolution is responsible for all that we see around us,
> > > what mechanism was used to produce such diversity of form and
function?
> >
> > Natural Selection of variations. But you already know that
> >
> > > Where are your numbers to back up the creative potential of such a
> > > mechanism?
> >
> > Who needs numbers when the planet is literally crawling with directly
> > observed examples?
>
> Hmmmmm. You have a point. The problem is that these directly observed
> examples never go beyond the 1000aa threshold of specifically arranged
> residues.
So what? Why would that be a problem?
> All of the examples out there are significantly lower-level
> than 1000aa. Now why is that? What is it that prevents there being
> any examples beyond this level?
Why do you think they need to exceed that threshold, other than reasons of
personal incredulity?
> What is the statistical reason for
> this phenomenon?
Stats are a tool, they don't provide "reasons".
Boikat
Seanpit
> Marc wrote:
< snip >
> Wait a minute here.
>
> Your "evolutionary" process of B-cells undergoing somatic
> hypermutation is actually more a stage of development than
> it is a process of evolution.
LOL - You just never give up do you? No matter how many of those even
from your own side of this issue challenge you on this point you hang
in there. Admirable, even if not correct.
> Over the course of evolution of
> the vertebrate adaptive immunity the specfic mechanism
> of hypermutation developed with specific enzymes that
> target only certain regions of the antibody binding pocket.
> Yes, there is "selection" of some cells over others so concepts
> of evolution can apply, but to call this process the same as
> mainstream "random mutation evolution of the species" is
> bogus and to use a supposed failing of somation hypermutation
> to perform as real evolution is a false argument (a "lie", dude)
> as you use it on your site.
Many on this forum, even those on your own side when it comes to being
an evolutionist, agree with me on this one. There is no fundamental
different when it comes to mechanism. B-cells undergo random mutations
and function-based selection over generations within the environment of
a human individual. In this situation, B-cells are indeed equivalent
to the "species" and they do indeed undergo functional evolution. This
is not a "lie" as you call it. It is a fact. It just amazes me how you
can continue to argue this point given your background as an
immunologist and given the information you've been given in this forum.
> Please tell my why the explicit term is "SOMATIC hypermutation",
> and why that extremely fast mutation rate is *not* the rate cited
> as the mutation rate for evolution outside of B-cell CDR3 regions.
The term somatic is used because that is the type of cell or "creature"
that is undergoing random mutation. It doesn't matter if this is
happening in a somatic cell or a germ cell. The mechanism is the same.
There is no fundamental difference. The difference is rate is just
that, a difference in rate. Some creatures "evolve" more rapidly than
do others. The rate of computer code evolution could be even faster.
Yet, it would still be called "evolution" because of the use of the
very same mechanism of random mutation and function-based selection.
Evolution isn't defined by the rate of mutation. It is defined by
mutations of whatever rate combined with function-based selection. Any
living or non-living thing that is using that mechanism is undergoing
true evolution. It really isn't more complicated than that.
> When cells undergo planned processes within the body that use
> specific enzymes to make changes in just certain sites, and when
> this process does not contribute to future generations or even build
> on itself (somatic hypermutation only happens at very specific and
> limited stages in a B-cell's life, and it does not go on and on), it is
> more a process of developmental biology than it is evolutionary
> biology. I have accepted that tumours which beging to be passed
> between members of a species (as in dogsa and tassie devils) are
> across the threshold of becoming an entity that is "evolving", so
> you should learn to accept when you are wrong, too.
You are wrong on both accounts. It doesn't matter if a life form is
passed on or not or if it continues to evolve or not. All that is
needed to qualify as "evolution" is random mutation and function-based
selection over many or even a very few generations of that particular
life form (B-cells in this case). Nothing else is required Marc. I
dare say that the majority of those even within this forum would
disagree with your definitions here. Test it out and see if you don't
believe me. Ask for a vote why don't you?
> Another point - you make one of your "trillions of" type arguments
> on your immunity page about the combinational diversity of the
> antibodies but the problem is your calculations concern the
> framework of the molecule and not the binding site. That is,
> you use the "large numbers" argument as if that large diversity
> was in fact in the antigen binding pockets, which it is not. Binding
> sites are what is important but you ignore them and you also
> ignore the limits of specificity by not allowing for any degree
> of cross-reactivity or mimicry in antigen recognition. If you have
> false arguments to base your conclusions on, what does that
> say about your conclusions, "doctor"?
Differences in the various segments of the antibody affect
antibody-binding activity. "The diversity generated by this mechanism
in the variable region of the heavy chain - to be specific, in the area
that these V, D and J genes encode, otherwise known as the
complementarity determining region 3 (CDR3) - provides the human immune
system its ability to bind so many distinct antigens." (Ref 1).
"As the table shows, this lays the foundation for a potential B-cell
repertoire of 2.5 x 10^6 different antibody V regions. But the true
number is probably virtually limitless because of:
1. variation in the exact splice point and
2. the introduction of N nucleotides
3. both of which increase the diversity of CDR3."
Ref 2
"The first level is variable diversity joining (VDJ) recombination, in
which gene fragments are rearranged to encode functional antibodies,
producing a range of antibodies with a diversity on the order of 10^12
to 10^14. Upon invasion of the body by a foreign antigen, the second
level of B cell somatic hypermutation evolution is initiated, in which
division, mutation, and selection of B cells occurs. Those B cells that
produce antibodies that bind the antigen with higher affinities are
selected and propagated. Thus, the individual point mutations of
somatic hypermutation essentially perform an optimizing local search of
amino acid sequence space." (Ref 3)
References:
1. http://en.wikipedia.org/wiki/Antibody
2.
http://home.comcast.net/~john.kimball1/BiologyPages/A/AgReceptorDiversity.html
3. http://www.mwdeem.rice.edu/djearl/autoimmune.pdf
I deal specifically with the epitope variety question, as in the
following passage:
"Each educated T-cell has only one type of receptor so only one
specific antigen can be recognized. But, how many possible antigens
are there? 'The total number of possible epitopes is, therefore, 20^B
since there are 20 different amino acids.' Well, the typical length of
an antigen epitope ("B" in the preceding formula) is about 20 amino
acid residues. So, the total number of possible antigen epitopes is
about 20^20 or 104,857,600,000,000,000,000,000,000 or ~100 trillion
trillion."
Jun Sun, David J. Earl, and Michael W. Deem, Glassy Dynamics in the
Adaptive Immune Response Prevents Autoimmune Disease, Physical Review
Letters, 95, 148104, September 30, 2005
(http://www.mwdeem.rice.edu/djearl/autoimmune.pdf)
As it turns out, the odds that an antibody will bind or "recognize" a
random epitope to at least some degree of useful affinity is about
1e-12 (or 1 in a trillion). Approximately the same is true for TCRs.
This gives a fairly good hint at the diversity capability of the vast
array of epitope recognition by antibodies and T-cell receptors as well
as the minimum number of potentially different antibodies and receptors
produced by the total compliment of T- and B-cells in the human immune
system.
If you disagree to any significant degree with these numbers, I'd be
most interested in your own estimate of antibody and TCR variability
and antigen epitope recognition.
> (signed) marc
Sean Pitman
www.DetectingDesign.com
Seanpit
John Harshman wrote:
> Seanpit wrote:
>
> >>>>Sean Pitman wrote:
> >>>
> >>>Marc wrote:
> >>
> >>John Harshman wrote:
> >
> >
> >>>>For my part, I've already shown you, over and over again, that gene
> >>>>duplications do not produce any novel function at all.
> >>>
> >>>You have not *SHOWN* any such thing. You *have* declared it,
> >>>you have *assumed* it, you have cried it from mountain tops, but
> >>>you have *never* _shown_ it and you can't. You're wrong and you
> >>>have to LIE to "show" it.
> >
> > I've shown you the statistical reasons why your assumption of
> > evolutionary mechanisms doing what you think they did just isn't
> > tenable this side of trillions upon trillions of years of time. You
> > have yet to counter with any relevant statistical analysis of your own
> > with regard to the potential of your proposed mechanism. You simply
> > assume that your mechanism did the job in relatively short order
> > without any statistical backing whatsoever with regard to the workings
> > of your actual mechanism.
>
> No, he shows that the job was done. I don't think we've arrived at the
> question of mechanism yet.
This entire discussion is about mechanism John. If the mechanism isn't
tenable, then your assumption of evolution isn't tenable either. Slow
creation isn't the same thing as common descent.
> First we have to establish that such things
> have happened in the history of life, which the evidence does establish.
All the evidence establishes is that a particular pattern exists - a
pattern of nested hierarchy for certain features in certain creatures
(not universal however). I discuss this hierarchical pattern and the
assumptions behind it further below (as I have many times before with
you).
> And it's clear that gene duplication has been an important part of that
> process.
Given the a priori assumption actually happened via mindless
evolutionary processes, then it is clear that gene duplications were
involved. However, the entire question is the original assumption that
gene duplications without the aid of ID could have reasonably done the
job within just a few billion years.
> Until we can agree on basics like that, we can't even begin to
> address mechanism, because you will reject all the relevant evidence.
See discussion of pattern assumptions below . . .
> I predict that once again you will ignore questions of phylogeny in
> favor of reiterating your "neutral gap" claims.
How you can make this "ignore" prediction is beyond me since I've
discussed this logical fallacy of yours many times before in this
forum.
> I predict also that you will ignore the independence of common descent
> and intelligent design, claiming by elision that your neutral gap theory
> falsifies common descent.
Likewise, slow stepwise creation, if that is indeed what happened, is
not the same thing as common descent. Common descent implies both
common ancestry and variation over time via evolutionary mechanisms.
Anything else is simply slow creation, with preservation of design.
Preservation of design is just good design be the overall creation
rapid or extended over a long period of time. Using the same or nearly
the same genetic codes in different creatures to do various functions
is quite handy and aesthetically attractive. Why reinvent the wheel
all the time?
> >>>Every paper I cited in the other reply in this thread, every paper
> >>>that was cited to you Nov. 21st and every paper cited months
> >>>before that *SHOWS* that duplication of genes or genomes leads
> >>>to new functions in the protein family concerned. Every report says
> >>>something about a different protein family or in a different species
> >>>and they all have the same theme (which you dismiss because
> >>>you don't like sequence data being studied).
> >>
> >>All this is inferred from gene or organismal phylogenies. Sean doesn't
> >>believe in phylogenies. He's a creationist. And he thinks that his
> >>personal disbelief allows him to reject the evidence out of hand.
> >>
> >>What Sean is asking for is for a gene duplication to evolve into
> >>multiple functions while he watches. Absence of such events falsifies
> >>evolution (in his world, where the sky is a lovely shade of violet).
> >>
> >>(Behe takes a similar position on ID; though he accepts common descent,
> >>unlike Sean, he does demand that scientists grow flagellae on bacteria
> >>while he watches.)
> >
> >
> > I've said many times before that the demonstration of just a single
> > proposed step (beyond the 1000aa threshold) in the evolution of a
> > function as complex as flagellar motility would be enough to falsify my
> > position. What is most interesting here is that functions with lower
> > structural threshold requirements evolve all the time. Why is it then
> > that functions with a few more structural threshold requirements, only
> > 1000aa, do not evolve in real time at all?
>
> Because you're making up a criterion that nobody else can figure out?
Oh please. I've not made up these very simple and obvious criteria at
all. They are clearly demonstrated in scientific literature.
Functions requiring a minimum threshold of less than 1000 specifically
arranged residues evolve all the time while none beyond this level have
ever been shown to evolve at all. Does this fact really confuse you?
Really?
> > Very simple functions do
> > evolve with those with a bit more complexity do not evolve with a
> > spectrum of the stalling-out effect in between. What's your
> > explanation?
>
> You made it up?
Look it up. It's an easily verifiable fact.
> > I mean really, if the individual steps are not separated
> > by sizable gaps, non-beneficial gaps that are significantly wider than
> > they are at lower levels, what is it that prevents a flagellar motility
> > system from evolving right before our eyes?
>
> The question is meaningless. It turns all the complexity of evolution
> into a ridiculously simple model with invented parameters.
See, the model is "simple" after all. You describe it as "difficult to
figure out". Yet, it is in fact "ridiculously simple" with very clear
parameters. All one has to do to verify what is going on is look at
the scientific literature and see that functions with a minimum
threshold limitation of less than 1000aa evolve all the time while
functions with a greater threshold requirement simply do not evolve at
all.
Come on now John, answer the question. If there are no gaps between
the proposed steps of flagellar evolution, why doesn't it or anything
equivalent ever happen in real time?
> But you are distracting attention from the point here, which is that you
> refuse to accept the evidence of past evolution. On what basis?
Upon the basis that evolution isn't the only potential mechanism. Your
entire position is based upon the notion that, "No intelligent designer
would have made it that way." That's a philosophical position, not a
scientific position. You have to be able to test that philosophical
basis in a falsifiable way before it becomes a scientific position.
The truth of the matter is that both ID and evolutionary mechanisms can
produce hierarchical patterns. Therefore, the mere existence of such a
pattern does not favor one mechanism over the other as the actual
cause. There are other characteristics involved. In order to support
the evolutionary mechanism over ID, you have to show that the
evolutionary mechanism can explain these other features as well as the
overall hierarchical pattern. The main feature that seems beyond the
evolutionary mechanism is the feature of functions that go far beyond
the 1000aa threshold. This particular feature cannot be reasonably
explained by the proposed evolutionary mechanisms, but remain within
the realm of ID.
Pattern isn't enough to exclude the ID-only hypothesis. You have to do
better than that John.
Sean Pitman
www.DetectingDesign.com
Seanpit
Tell that to the guys running Las Vegas . . .
>
> Boikat
Seanpit
Ye Old One wrote:
> >> The fact is that about 4 billion years ago life started on Earth. From
> >> then to now we have a process called evolution that has, in response
> >> to the environmental pressures, produced the diversity of life we see
> >> around us today.
> >>
> >> You can't put numbers to evolution, it is not a number based process.
> >
> >All truly scientific hypotheses are based on predictive value, which is
> >a numbers based value. If you can't evaluate the abilities of your
> >proposed mechanism, statistically, how can you say that this mechanism
> >is more or less likely than any other potential mechanism? Hmmmmm?
> >You need numbers my man. Where are they?
>
> Life exists, in great diversity. All that life has evolved from
> earlier life over the last 4 billion years. Where do you see the need
> for numbers in that?
That's a nice hypothesis. What predictive value does it have in order
to support the notion that it is better than any other potential
hypothesis to explain such diversity of life? In short, what is it
that makes your theory subject to potential falsification? You see,
you do in fact need statistics and numbers before you can say that your
theory is likely "better" than any other potential hypothesis or
theory.
Look it up. All scientific hypotheses require the support of
statistically determined predictive value (i.e., numbers).
> Bob.
Sean Pitman
www.DetectingDesign.com
John Harshman
Depends on what you mean by "slow creation", which is so far an
undefined term. What do you mean? And whatever you mean, is that what
you think happened?
>>First we have to establish that such things
>>have happened in the history of life, which the evidence does establish.
>
> All the evidence establishes is that a particular pattern exists - a
> pattern of nested hierarchy for certain features in certain creatures
> (not universal however). I discuss this hierarchical pattern and the
> assumptions behind it further below (as I have many times before with
> you).
But you have never presented any reason for that pattern other than a
hand-wave in the direction of "common creator". I hope you'll do better
this time, though I'm not optimistic.
>>And it's clear that gene duplication has been an important part of that
>>process.
>
> Given the a priori assumption actually happened via mindless
> evolutionary processes, then it is clear that gene duplications were
> involved. However, the entire question is the original assumption that
> gene duplications without the aid of ID could have reasonably done the
> job within just a few billion years.
No, you are still confusing common descent with mindless processes. The
two are not necessarily connected. This is a consistent failure of
imagination on your part.
>>Until we can agree on basics like that, we can't even begin to
>>address mechanism, because you will reject all the relevant evidence.
>
>
> See discussion of pattern assumptions below . . .
>
>
>>I predict that once again you will ignore questions of phylogeny in
>>favor of reiterating your "neutral gap" claims.
>
> How you can make this "ignore" prediction is beyond me since I've
> discussed this logical fallacy of yours many times before in this
> forum.
What you call "discussed" I call "handwaving", and it's hardly been
reasonable.
>>I predict also that you will ignore the independence of common descent
>>and intelligent design, claiming by elision that your neutral gap theory
>>falsifies common descent.
>
> Likewise, slow stepwise creation, if that is indeed what happened, is
> not the same thing as common descent. Common descent implies both
> common ancestry and variation over time via evolutionary mechanisms.
No. Common descent implies only common ancestry. That's what the words mean.
> Anything else is simply slow creation, with preservation of design.
> Preservation of design is just good design be the overall creation
> rapid or extended over a long period of time. Using the same or nearly
> the same genetic codes in different creatures to do various functions
> is quite handy and aesthetically attractive. Why reinvent the wheel
> all the time?
This has been one of your fallback defenses. But it doesn't explain the
nested hierarchy in neutral features, nor does it explain why the
hierarchy is so seldom violated. A real designer uses good ideas
whenever he needs them; but life has indeed "reinvented the wheel" many
times, as in, for example, the wings of birds, bats, and pterosaurs,
each constructed from a tetrapod forelimb but in radically different ways.
So are you admitting that common descent is indeed a real phenomenon,
but claiming that its mechanism is intelligent (as Michael Behe does) or
are you trying to remain as vague as possible about the consequences of
the data?
Yes. "Specifically arranged" seems to be the major source of vagueness.
How do you know which residues are specifically arranged and which
aren't? How many of the residues in cytochrome b, for example, are
specifically arranged? Which ones?
>>Very simple functions do
>>>evolve with those with a bit more complexity do not evolve with a
>>>spectrum of the stalling-out effect in between. What's your
>>>explanation?
>>
>>You made it up?
>
> Look it up. It's an easily verifiable fact.
Look what up? Where?
>>>I mean really, if the individual steps are not separated
>>>by sizable gaps, non-beneficial gaps that are significantly wider than
>>>they are at lower levels, what is it that prevents a flagellar motility
>>>system from evolving right before our eyes?
>>
>>The question is meaningless. It turns all the complexity of evolution
>>into a ridiculously simple model with invented parameters.
>
> See, the model is "simple" after all. You describe it as "difficult to
> figure out". Yet, it is in fact "ridiculously simple" with very clear
> parameters. All one has to do to verify what is going on is look at
> the scientific literature and see that functions with a minimum
> threshold limitation of less than 1000aa evolve all the time while
> functions with a greater threshold requirement simply do not evolve at
> all.
What is a "minimum threshold limitation"? And what happened to the
qualifier "specifically arranged"?
> Come on now John, answer the question. If there are no gaps between
> the proposed steps of flagellar evolution, why doesn't it or anything
> equivalent ever happen in real time?
I have offered reasons before. The history of life is convoluted. There
is commonly no direct path from A to Z, and big changes commonly happen
in fits and starts, as one selected change alters the selective
environment and opens up another short path to another change, etc. So A
goes to B, which opens up the possibility of C, and an environmental
change opens up the path to D, and so on. Thus you find (my favorite
example) your middle ear bones to be constructed from what was once the
support for a filter feeding apparatus, with stops at breathing and
biting along the way.
>>But you are distracting attention from the point here, which is that you
>>refuse to accept the evidence of past evolution. On what basis?
>
> Upon the basis that evolution isn't the only potential mechanism. Your
> entire position is based upon the notion that, "No intelligent designer
> would have made it that way." That's a philosophical position, not a
> scientific position. You have to be able to test that philosophical
> basis in a falsifiable way before it becomes a scientific position.
No, I make no assumption about existence or nonexistence of an
intelligent designer in finding a nested hierarchy as evidence of common
descent. I make only two assumptions about his/her/its nature (if it
exists): first, that it isn't trying to fool us; second, that it's
unlikely to have chosen, out of all the myriad ways of creation, the one
way that matches the expectations of common descent, especially the
features that are totally senseless, like that nested hierarchy in
silent sites. This shows that the creator, if there is one, used common
descent. It may conceivably have purposely caused some few particular
mutations, but most of them were random, neutral, and neutrally fixed.
> The truth of the matter is that both ID and evolutionary mechanisms can
> produce hierarchical patterns.
Not that I have ever seen. Show me a nested hierarchy that doesn't
involve common descent.
> Therefore, the mere existence of such a
> pattern does not favor one mechanism over the other as the actual
> cause.
Only if you can show me such a hierarchy. You have merely claimed they
exist. Attempts at examples have failed.
> There are other characteristics involved. In order to support
> the evolutionary mechanism over ID, you have to show that the
> evolutionary mechanism can explain these other features as well as the
> overall hierarchical pattern.
Once again, you confuse common descent with natural selection.
> The main feature that seems beyond the
> evolutionary mechanism is the feature of functions that go far beyond
> the 1000aa threshold. This particular feature cannot be reasonably
> explained by the proposed evolutionary mechanisms, but remain within
> the realm of ID.
> Pattern isn't enough to exclude the ID-only hypothesis. You have to do
> better than that John.
I agree that a nested hierarchy is not enough to exclude the ID
hypothesis. I'm not sure what you mean by "ID-only". Sometimes I suspect
you are being purposely vague. Perhaps you could recount in detail what
you think actually happened. What did the creator do? I don't mean what
sort of magic he used, but what events he caused to happen and in what
order. Did he in fact incorporate common descent? If not, where does
that nested hierarchy actually come from? I maintain that only common
descent explains the nested hierarchy of life, regardless of whether ID
explains complex structures. The only potentially viable ID models must
incorporate common descent or they will be easily falsified by the edata.
This attempt to deal with nested hierarchy is just another repetition of
your previous lame attempts. It suffers from many fatal flaws:
1. Imprecision in use of words, so that I can't tell what you are really
claiming. You need to present a model that at least approaches one
that's as detailed as mine.
2. Conflation of common descent with natural mechanisms, driven by your
constant attempts to turn the discussion back to your beloved "neutral
gaps".
3. Avoidance of important questions, such as the nested hierarchy in
neutral sites.
4. Claims of facts not in evidence, such as known created (but "natural"
in the technical sense) nested hierarchies.
5. Failure to face up to the differences between your model, human
design and construction, and the hierarchy of life -- indicated by the
discussion above about "reinventing the wheel".
ouroboros rex
>
> ouroboros rex wrote:
>
>> >> >> There are a lot of cells out there, doctor.
>> >> >
>> >> > The calculations assume a population the size of all the bacteria on
>> >> > Earth (about 1e30). Massive population sizes really don't solve the
>> >> > problem - not even remotely close.
>> >>
>> >> I'd be interested in seeing those.
>> >
>> > Go to: http://www.detectingdesign.com/flagellum.html
>> >
>> > In the "Table of Contents", click on the link for "Trillions upon
>> > Trillions of Years". Then, in the first paragraph, click on the link
>> > for "calculation".
>> >
>> > Sean Pitman
>> > www.DetectingDesign.com
>>
>> I'm afraid that page is worthless, for too many reasons to go into
>> here -
>> opaque writing, unexplained assumptions, bad case limitations, etc., etc.
>
> Did you actually read the entire essay?
No, I went to the page you indicated, using your instructions.
If so, what unexplained
> assumptions and limitations, specifically, need additional help?
Well, I'm not qualified to generate a complete list. Let's start with
that 1000-residue requirement. Where's it come from, and could it ever
exclude an example that disproves your threshold theory (which I'm afraid
still confuses me, BTW)?
Cites for the work you build upon might be nice too.
>
>> Do you have a real cite?
>
> As far as I am aware, no one else is presenting this particular view.
Ah. In that case, could I get something on my other post? I'm still
trying to grasp your actual claims.
"Seanpit" <seanpi...@naturalselection.0catch.com> wrote in message
news:1167857338.8...@v33g2000cwv.googlegroups.com...
>
>
> The ratio decreases exponentially with each step up the minimum
> structural threshold ladder of functional complexity.
Google appears to find no evidence for the existence of this concept other
than your own writings, what else do you have? Not being a scientist or MD,
my search options are somewhat limited.
Is this why your 'calculations' page has those initial constrictions, like
bullpup
Playing odds is not a "reason" either. Gamblers use stats (odds) to guide
their play, but not the other way around. Gamblers do not gamble because
there are stats around to base their odds of winning on.
Boikat
JTEM
Seanpit wrote:
> Are you arguing that the process of intelligent design
> is "magic"?
No more or less so than invisible pink unicorns.
If you don't mind, I'm just going to delete the rest of your
bullshit without comment.
wf3h
Seanpit wrote:
> nickm...@gmail.com wrote:
> > >
> > In other words, Sean thinks:
> >
> > 1 protein: possible
> > 2 proteins (under 1,000 aas): possible
> > 3 proteins (over 1,000 aas): absolutely impossible and therefore
> > evidence of divine intervention.
>
> This is correct; except for the part about divine intervention. Any
> high-level intelligence could produce the same type of creation.
really?
1.how?
2. how do you know this?
It
> doesn't have to be the result of divine intelligence, just deliberate
> intelligent activity of some kind that goes far beyond the realm of
> what random mutation and function-based selection can achieve.
ah. so some mystical, magical, but natural scientific force is
involved. and that proves no natural forces were involved
uh huh...
sean...you obviously learned nothing in the lab.
wf3h
Seanpit wrote:
> JTEM wrote:
> >> > 25 years ago we couldn't "Explain" how people got
> > AIDS. There were some who suspected a virus, even
> > some who believed it was sexually transmitted, but
> > nobody really knew.
> >> Are you arguing that the process of intelligent design is "magic"?
> What about your own creative abilities? Are they "magical"?
well, that seems to be YOUR argument.
intelligence uses ONLY natural laws for expression. intelligence can
NEVER violate natural law..except creationists say it can.
proof? why...none...none at all.
If you
> can't remotely explain how your mindless mechanism can do the job, then
> you have to at least consider the possibility that IDists just might
> have something - that there just might be significant limitations
> behind your proposed mechanism.
and what is their mindful mechanism? seems creationists dont have any
more answers than science does...they just use god to not explain
anything.
>
Marc
Seanpit wrote:
> > Marc wrote:
> < snip >
>
> > Wait a minute here.
> >
> > Your "evolutionary" process of B-cells undergoing somatic
> > hypermutation is actually more a stage of development than
> > it is a process of evolution.
>
> LOL - You just never give up do you? No matter how many of those even
> from your own side of this issue challenge you on this point you hang
> in there. Admirable, even if not correct.
It does not matter if any here agree or not - most of them (like you)
are not immunologists, are they? And, as an immunologist, the
points I am making are factual and are correct. B-cell mutations
are a "developmental" process that evolved to use specific changes
to a binding site and selection as a mechanism to improve the
binding of some antibodies. Whilst this is in fact "evolving" an
immune response, it is NOT the process of evolution itself and
your web-page argument is false logic in this regard. You can't
take a process that is NOT "evolution" and point to it's failure to
move beyond a certain point and then say "See? Evolution doesn't
go past this point. Nothing more than a better antobody comes from
this thing called evolution." - That is what your argument is, and
this is why it is wrong to use it that way.
> > Over the course of evolution of
> > the vertebrate adaptive immunity the specfic mechanism
> > of hypermutation developed with specific enzymes that
> > target only certain regions of the antibody binding pocket.
> > Yes, there is "selection" of some cells over others so concepts
> > of evolution can apply, but to call this process the same as
> > mainstream "random mutation evolution of the species" is
> > bogus and to use a supposed failing of somation hypermutation
> > to perform as real evolution is a false argument (a "lie", dude)
> > as you use it on your site.
>
> Many on this forum, even those on your own side when it comes to being
> an evolutionist, agree with me on this one.
Again, it does not matter if Glenn or spintronic agree with me. While
I do respect the comments of Harshman and Wilkins, and there is an
aspect of evolution in the somatic hypermutation (SM) process, there is
also a great deal of control over the process of SM and it is limited
to
a very short window in the life of a B-cell - it is not the ongoing
process
that you are making it out to be, and the mutations do not get passed
on in the germline. By your logic then every change in every cell in
the
body over development would be "evolution", so where does that sort
of normal cellular "evolution" end? If a B-cell only mutates certain
residues and only does so with a specific enzyme and only does
so at a critical point after it has been involved in an immune response
and this only happens for the one time in it's life, where is there
any formal "evolution" in that process? I have always accepted that
"the immune response evolves" but to make blanket statements
about the rest of what evolution does throughout biology based
on this one very specific, limited example is a falsehood by you.
> There is no fundamental
> different when it comes to mechanism.
The B-cells use an enzyme to create their specific "mutations"
and do so in quite controlled ways - I'll cite the papers later (and
they have been cited before), they do not collect these mutations
by any of the processes of mutation that occur in every other
arena that evolution is taking place in. Thus, there is in fact a
very big difference in mechanism. B-cells do their "mutations"
in a specific manner that does not happen anywhere else.
> B-cells undergo random mutations
> and function-based selection over generations within the environment of
> a human individual.
Not "over generations" in the sense you are trying to say here.
Again, you are pushing an argument past the point of truth.
> In this situation, B-cells are indeed equivalent
> to the "species" and they do indeed undergo functional evolution. This
> is not a "lie" as you call it. It is a fact. It just amazes me how you
> can continue to argue this point given your background as an
> immunologist and given the information you've been given in this forum.
The information in this forum - your comments and those of a couple
of others - do not stand up to the biomedical literature which has
the facts as I am presenting them. Don't blame Dr. Max for you
taking his argument out of context and explaining it badly to me.
> > Please tell my why the explicit term is "SOMATIC hypermutation",
> > and why that extremely fast mutation rate is *not* the rate cited
> > as the mutation rate for evolution outside of B-cell CDR3 regions.
>
> The term somatic is used because that is the type of cell or "creature"
> that is undergoing random mutation. It doesn't matter if this is
> happening in a somatic cell or a germ cell.
You fail the test here also - the term "somatic" means that the
mutations do not enter the germline and are not passed to the
next generation of whichever vertebrate organism you consider.
> The mechanism is the same.
> There is no fundamental difference. The difference is rate is just
> that, a difference in rate. Some creatures "evolve" more rapidly than
> do others. The rate of computer code evolution could be even faster.
Examples about "computer codes" are bogus arguments with
respect to biological evolution.
> Yet, it would still be called "evolution" because of the use of the
> very same mechanism of random mutation and function-based selection.
But B-cells have their own specific mechanism to make any changes,
so it is NOT "the very same" as mutation elsewhere, is it?
> Evolution isn't defined by the rate of mutation. It is defined by
> mutations of whatever rate combined with function-based selection. Any
> living or non-living thing that is using that mechanism is undergoing
> true evolution. It really isn't more complicated than that.
They why do you not grasp that you are in error?
> > When cells undergo planned processes within the body that use
> > specific enzymes to make changes in just certain sites, and when
> > this process does not contribute to future generations or even build
> > on itself (somatic hypermutation only happens at very specific and
> > limited stages in a B-cell's life, and it does not go on and on), it is
> > more a process of developmental biology than it is evolutionary
> > biology. I have accepted that tumours which beging to be passed
> > between members of a species (as in dogs and tassie devils) are
> > across the threshold of becoming an entity that is "evolving", so
> > you should learn to accept when you are wrong, too.
>
> You are wrong on both accounts. It doesn't matter if a life form is
> passed on or not or if it continues to evolve or not. All that is
> needed to qualify as "evolution" is random mutation and function-based
> selection over many or even a very few generations of that particular
> life form (B-cells in this case).
Here you sneak back to "a very few" generations, when you *really*
need to edge back to just "a couple" in fact - and in doing this you
have had to create a "life form" out of B-cells. Again, is every cell
in the body a different "life form" [Yes, John... and John... there
are all sorts of other life forms within the body, but how many of
those gut flora and such are encoded in the vertebrate genome?]
> Nothing else is required Marc. I
> dare say that the majority of those even within this forum would
> disagree with your definitions here. Test it out and see if you don't
> believe me. Ask for a vote why don't you?
A vote means nothing, and the discussion has gone on a fair bit
with respect to tumours and so forth - I agree about some of those
points but stress that my argument here is based on the use of
this mutation/evolution stuff you make on your web site. When
you admit that you are using false logic there I will back off on
the issue here.
Any further comment on material snipped from below will have
to wait - we have kids to take to a party and the family awaits.
(signed) marc
nickm...@gmail.com
I'm glad I characterized your position correctly. So, please clarify
for us why you think two proteins can evolve to interact, but a third
protein could not evolve to interact with a preexisting two-protein
system?
Nick
nickm...@gmail.com
1000 required aas? If it does, your oft-repeated position is sunk, and
you have retreated to some other magical barrier to evolution.
Nick
Seanpit wrote:
> P.S. You wouldn't be the same Nick Matzke who wrote the essay on
> flagellar evolution would you? "Evolution in (Brownian) space: a model
> for the origin of the bacterial flagellum"?
Yep.
nickm...@gmail.com
Seanpit wrote:
> nickm...@gmail.com wrote:
> > sea...@naturalselection.0catch.com wrote:
> > > It is just that the odds for successful cooptation become
> > > exponentially more and more remote as you move up the ladder of
> > > functional complexity.
> >
> > Wild, undocumented, and clueless assertion. Bird wings are pretty
> > freaking complex, yet they have changed function multiple times in
> > various birds into flippers (penguins, flightless cormorant, giant auk,
> > etc.)
>
> So, the minimum size and complexity for the directed beneficial
> swimming function requires a fairly sizable degree of part and
> specificity requirements? Is that what you are trying to say?
No, I'm saying your claim that "the odds for successful cooptation
become exponentially more and more remote as you move up the ladder of
functional complexity" is bogus.
It's bogus because even extremely complex systems, i.e. flightless bird
flippers (which consist of multiple tissues, billions of cells, each
cell much more complex than a bacterium, let alone a bacterial
flagellum), have clearly changed function in relatively recent
evolutionary history.
> Come on now Nick. Show many any molecular system where all the parts
> work together at the same time beyond a minimum threshold level of 1000
> specifically arranged residues evolving in real time.
Why a molecular system? Do you disagree that a bird wing is more
complex than a bacterium?
> Your bird
> example isn't one of them because the threshold requirements a minimum
> selectable abilities were already in place ahead of time.
This sentence ain't grammatical, but I think what you are trying to do
is just insert yet another ad hoc excuse to save your argument.
Nick
>
> > Nick
>
> Sean Pitman
> www.DetectingDesign.com
John Wilkins
> Yes, John... and John... there
> are all sorts of other life forms within the body, but how many of
> those gut flora and such are encoded in the vertebrate genome?]
Now we're talking about endosymbiotic capture...
And yes, it's an evolutionary process. [I'll shut up now...]
--
John S. Wilkins, Postdoctoral Research Fellow, Biohumanities Project
University of Queensland - Blog: scienceblogs.com/evolvingthoughts
"He used... sarcasm. He knew all the tricks, dramatic irony, metaphor,
bathos, puns, parody, litotes and... satire. He was vicious."
wf3h
> .
>
> All truly scientific hypotheses are based on predictive value, which is
> a numbers based value. If you can't evaluate the abilities of your
> proposed mechanism, statistically, how can you say that this mechanism
> is more or less likely than any other potential mechanism? Hmmmmm?
> You need numbers my man. Where are they?
>
and ID has what mechanism?
oh. only YOUR mechanism doesn't need to be explained. your rule applies
to everyone but you, it seems
thanks, sean. explains alot.
wf3h
Seanpit wrote:
>>
> Likewise, slow stepwise creation, if that is indeed what happened, is
> not the same thing as common descent. Common descent implies both
> common ancestry and variation over time via evolutionary mechanisms.
> Anything else is simply slow creation, with preservation of design.
> Preservation of design is just good design be the overall creation
> rapid or extended over a long period of time. Using the same or nearly
> the same genetic codes in different creatures to do various functions
> is quite handy and aesthetically attractive. Why reinvent the wheel
> all the time?
why not? this is the problem with trying to out guess god. you can make
god do anything you want. that's why god is scientifically useless,
whereas evolution, with its mechanism, is a good scientific theory.
> > >
> Upon the basis that evolution isn't the only potential mechanism. Your
> entire position is based upon the notion that, "No intelligent designer
> would have made it that way." That's a philosophical position, not a
> scientific position. You have to be able to test that philosophical
> basis in a falsifiable way before it becomes a scientific position.
uh huh. and your position is that a designer WOULD make it the burger
king way...have it your way....that's a philosophical position if there
ever was one.
>
> The truth of the matter is that both ID and evolutionary mechanisms can
> produce hierarchical patterns.'
and the ID mechanism is?: you creationists keep pretending...yes,
pretending, there is one but you never tell us what it is.
Therefore, the mere existence of such a
> pattern does not favor one mechanism over the other as the actual
> cause. There are other characteristics involved. In order to support
> the evolutionary mechanism over ID, you have to show that the
> evolutionary mechanism can explain these other features as well as the
> overall hierarchical pattern. The main feature that seems beyond the
> evolutionary mechanism is the feature of functions that go far beyond
> the 1000aa threshold. This particular feature cannot be reasonably
> explained by the proposed evolutionary mechanisms, but remain within
> the realm of ID.
evolution, even by your standards, is the winner vs ID. you admit that
evolution can produce change BELOW the 1000aa threshold.
ID? how does IT do that? you don't say.
you merely assert it does. and that is meaningless.
>
> Pattern isn't enough to exclude the ID-only hypothesis. You have to do
> better than that John.
>
ID is not a hypothesis. saying that something violates natural law and
can therefore explain features in the natural world...which is the ID
position...is a scientific oxymoron.
Don Cates
[snip]
It seems to me that this is the main point against Sean's claim. IIUC,
the 'successful' immune cell does not become a new starting point for
further changes. In this way it is completely *unlike* biological
evolution and offers no support for Sean's ideas.
--
Don Cates ("he's a cunning rascal" - PN)
Seanpit
nickm...@gmail.com wrote:
> Does or does not the 2,4-DNT degradation system consist of more than
> 1000 required aas? If it does, your oft-repeated position is sunk, and
> you have retreated to some other magical barrier to evolution.
Did you bother to read the explanation? Of course not. Why snip it and
act like I said nothing in response? Why not actually respond to the
argument presented?
Yet again, such cascading pathways do indeed consist of more than
1000aa, but they are not all specifically arranged with all the other
residues in the system. The specificity requirement is therefore
lacking. The size requirement isn't the only requirement here. You
have to meet BOTH the size and specificity requirements.
> Nick
>
>
> Seanpit wrote:
> > P.S. You wouldn't be the same Nick Matzke who wrote the essay on
> > flagellar evolution would you? "Evolution in (Brownian) space: a model
> > for the origin of the bacterial flagellum"?
>
> Yep.
That's what I thought. I have to tell you that it is the best attempt
at explaining flagellar evolution that I have yet come across. Good
try! Really! ; )
http://www.detectingdesign.com/flagellum.html
Sean Pitman
www.DetectingDesign.com
Seanpit
It isn't so much the number of proteins, but the number of specifically
arranged amino acid residues that's the problem. Beyond the 1000aa
threshold no novel beneficial functions are evolved in real time. It
just doesn't happen (P.S. cascades don't satisfy the specificity
requirement).
The seemingly obvious explanation for this phenomenon is the
exponentially expanding non-beneficial gap problem. A non-beneficial
gap exists between island clusters of potentially beneficial sequences
within sequence space. Higher level functions (i.e., those with
greater size AND specificity threshold requirements) have, on average,
a linear increase in the linear gap distance between potentially
beneficial sequences. A linear increase in gap distance translates
into an exponential increase in the number of mutations of any kind it
would take to cross this distance - on average.
> Nick
Sean Pitman
www.DetectingDesign.com
Seanpit
John Wilkins wrote:
> Marc <marcb...@aapt.net.au> wrote:
>
> > Yes, John... and John... there
> > are all sorts of other life forms within the body, but how many of
> > those gut flora and such are encoded in the vertebrate genome?]
>
> Now we're talking about endosymbiotic capture...
Right . . .
> And yes, it's an evolutionary process. [I'll shut up now...]
Yep . . .
Blodgett
> > > 2 proteins (under 1,000 aas): possible
> > > 3 proteins (over 1,000 aas): absolutely impossible and therefore
> > > evidence of divine intervention.
> > This is correct; except for the part about divine intervention. Any
> > high-level intelligence could produce the same type of creation.really?
Yes, if a major change to an organism were to be observed in a single
step: e.g. growth of a new functional useful limb or a a fish giving
birth to a mamal, this would be evidence of creationism.
Evolution predicts only very gradual change - for example mutations
typically directly affect only one gene at a time, and not many.
Seanpit
Oh please. The ability to swim through water isn't significantly
different from the ability to fly through air. If anything, its easier
to go from flying to swimming than visa versa. Nothing is really gained
here. This is like arguing that flightlessness or blindness is are
"new" functions when in reality these are nothing more than losses or
minor modifications of a pre-existing systems. What you are describing
here is more like a learned ability with minor subsequent body
modifications to improve the efficiency of an ability that was always
physically possible from the beginning.
> > > Nick
> >
> > Sean Pitman
> > www.DetectingDesign.com