Re: Direct Experimental Evidence for Non-Beneficial Gaps

Seanpit wrote:
On Jul 9, 6:46 am, John Harshman <jharshman.diespam...@xxxxxxxxxxx>
wrote:
Seanpit wrote:

That's a fundamental problem. It is the surrounding environment in
the form of other systems within the organism with which the system in
question must interact that put structural constraints on the system
in question. Not just any non-homologous arrangement of equivalent
size is going to be able to do the job. That is one of the main
reasons beyond the ratio estimates of those like Yockey, Sauer, and
Olsen, etc.
So we are all agreed that a random sequence of amino acids is very
unlikely to insert itself into a complex, existing system.

That's actually not all that unlikely. Essentially random stretches
of DNA often get inserted into various places within the genome at
random.

You persist in introducing irrelevant factoids. Why?

Of course the
complex, existing system wouldn't exist unless there was something
already filling that spot, so what does it matter? But that's a strawman
model of evolution. What if these relationships among proteins
evolved? The initial proteins would not have such constraints. You are
trying to disprove evolution using a static model.

The problem with this notion is that you can't evolve constraints
where the function in question was originally present without any
constraints. That's simply not possible. All functionally beneficial
systems require at least some minimum constraints to work. There is
simply no such thing as a functionally beneficial constraintless CytoC
function, or lactase, nylonase, flagellar, ATPase, etc function
without any constraints. That's just nonsense. If you start without
any constraints, you start at a functionless place. The gain of a
beneficial function entails the building of constraints.

Again you persist in misreading almost everything. I'm getting tired of it.

Come on John, these are published peer-reviewed estimates that are
unchallenged in literature. If you really think that these authors
were so far off base, the burden of evidence is really on you. What
evidence do you have to suggest that these estimates are likely to be
significantly off base? As far as I can tell, you've presented
nothing but incredulity without any real substance behind your
doubt.
I mean, what is your suggested ratio for CytoC functionality in
sequence space? Do you think it is likely to be as low as say, 1e-10
or maybe 1e-5? Do you really think this is at all likely given the
biological constraints of CytoC that are actually known?
I don't know, and neither do you. And that's the wrong question anyway.

Oh come on now. You most certainly do have a pretty good idea. You
just won't admit it directly. Did you actually read any of the papers
I listed for you?

I try to avoid it whenever possible.

You do realize that Yockey's statistical estimates were supported
experimentally by those like Olsen and Sauer? - with the use of
"cassette mutagenesis experiments"? In other words, a functional
sequence was experimentally mutated to the point of a loss of wild-
type function below a certain threshold of activity that would give a
selective advantage.

How was this threshold determined?

Based on the number of changes tolerated, the
total ratio of all possible sequences in sequence space was
estimated. For the case of lambda repressor function, Sauer and Olsen
estimated a ratio of around 1 in 1e65. This experimental finding
supports the finding of Yockey based on sequence variability analysis
in known sequences.

Do I really have to read this? Can't Howard do it? This may take a while.

http://www.tbiomed.com/content/pdf/1742-4682-4-47.pdf

More recently Axe (2004) has performed site directed mutagenesis
experiments on a 150-residue protein-folding domain within a B-
lactamase enzyme.

"Starting with a weakly functional sequence carrying this signature,
clusters of ten side-chains within the fold are replaced randomly,
within the boundaries of the signature, and tested for function. The
prevalence of low-level function in four such experiments indicates
that roughly one in 1e64 signature-consistent sequences forms a
working domain. Combined with the estimated prevalence of plausible
hydropathic patterns (for any fold) and of relevant folds for
particular functions, this implies the overall prevalence of sequences
performing a specific function by any domain-sized fold may be as low
as 1 in 1e77, adding to the body of evidence that functional folds
require highly extraordinary sequences."

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WK7-4CVV2GH-2&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=db953fac9eef182b969c83f102879a9a

These findings are based on direct experimental evidence that tests
the boundaries of functionality John. What more do you want besides
absolute proof? - which is impossible and not a requirement of
science?

Also consider a recent 2007 paper by Dursten et. al.

http://www.tbiomed.com/content/pdf/1742-4682-4-47.pdf

Using these very same ideas, Dursten actually proposes a mathematical
formula to estimate the "Functional Sequence Complexity (FSC)" of a
protein sequence. And, surprise surprise, there is a good correlation
between the size and sequence flexibility of a protein and Dursten's
FSC number. The greater the size and/or specificity of a protein, the
greater its FSC. See Figure 2:

http://www.tbiomed.com/content/download/figures/1742-4682-4-47-2.PDF

Again, this should be intuitively obvious to you, and I think it is.
This experimental and statistical evidence only cements the obvious.

Not at all, since you have absolutely no idea what the "ancestral
protein" might have looked like. The best evidence one has available
to estimate the ratio for a function like CytoC must be based on what
we actually know works.
Even if that estimate is logically invalid, for the reasons I have
stated? Sounds as if you're looking for your keys under the street light
because the light's better there.

You haven't stated any reasonable reasons. Several of your points are
completely wrong - to include your suggestion that the estimated ratio
do not account for weakly beneficial sequences, that they are only
based on sequence comparisons without testing for functionality, and
that there is absolutely no reasonable evidence to back up Yockey's
estimated ratios. You don't seem to be very informed on this
particular topic.

I agree that I haven't looked into it too deeply. But you have been unable to defend your claims either. Yockey's numbers do *not* count weakly beneficial sequences. They only count variation in existing sequences. If you disagree, how did Yockey account for suboptimal sequences?

If there were two unrelated non-homologous proteins of equivalent
minimum size requirements that both had at least some level of CytoC
functionality with a similar degree of specificity, the size of each
island would be equivalent in sequence space - as you note. What
would that do to Yockey's estimated ratio of 1e-65? What is 1e65
divided by 2? Is it not 1e64? Now, what does that really do to
Yockey's main point? Hmmmmm? What would a trillion (1e12) such non-
homologous CytoC islands do to Yockey's ratio? Change it to 1e-53?
Big deal - right? Do you still not see the statistical irrelevance of
your unlikely scenario? The point of the authors, that the ratio of
any sequence that has a particular function like CytoC vs. those that
have no useful level of that type of function, is very low.
That main point is overwhelmingly obvious and is unchallenged in
mainstream scientific literature.
Sorry, I forgot my math for a moment. Of course we don't know the
number. What, for example, if there were 10^55 such islands? Then we're
down to 10^-10. Since you have no way to estimate the number, one guess
is as good as another.

Not according to the above listed authors. Having 10^55 non-
homologous islands that have the same function at the level of a
minimum 100aa requirement or so is highly unlikely. Why? Because of
the previously mentioned biological constraints of an integrated
system in a particular larger biosystem or living thing. Some basic
homology at key positions for an equivalent sized protein would be
required for most functional systems in order to fit and work properly
in a particular organism or subsystem.

True, but of course this could be an entirely different homology from system to system.

Beyond this, experimental
results do not back up this suggestion of yours. All the available
experiments dealing with this issue strongly suggest far greater
island isolation for most protein-based systems of even a relatively
small protein like a 100aa protein.

At this point I have a choice either to believe your claims or look it up myself. I'm not sure which I'll do.

There are at least four reasons why Yockey's number doesn't do what you
want, even for cytochrome c.
1. It doesn't account for unrelated sequences with the same function.
Statistically irrelevant - - as noted above.
Only if the number of such sequences is small. You don't know if it's small.

Not with absolute certainty - no. Again, that's not required by
science. The available evidence, on the other hand, suggests that
your suggestion isn't remotely likely for the particular systems
analyzed by the listed authors.

I don't believe the listed authors actually addressed this question. Could you point to a passage that explicitly does that?

2. It doesn't account for related sequences that would do the same
function, but less well than extant ones.
Yes it does. You are wrong on this point. All of the authors,
especially Yockey, take into consideration any protein that would
perform the function in question to any useful degree vs. those that
would have no useful function of the type in question at all.
I don't see that, since Yockey's calculations, at least, are performed
by examining only the sequences in existing organisms. Are you saying
that some of these sequences are suboptimal?

That's exactly what I'm saying. Cassette mutagenesis by direct
experimentation and delineation of the boundaries of beneficial
functionality support this conclusion.

Let's be clear. Are you saying that Yockey's assay of existing sequences included a range of suboptimal sequences? How did he know they were suboptimal? Why were they not eliminated by selection?

3. It doesn't account for the sequences that would perform any function.
Nobody says that cytochrome c is necessary for life, or even for the
general function of getting energy out of food. If anything, you should
be asking how likely it is for a random protein to perform any useful
function whatsoever. We happened to get cytochrome c. In another world,
we might have something else entirely, functioning in some other system
entirely. You are pointing to the rarity of royal flushes in spades when
you should be calculating the chances of getting a hand better than that
of other players.
The relative rarity of particular types of functional systems in
sequence space can be used to estimate the overall rarity of all
potentially beneficial functions of all kinds at particular structural
minimum threshold requirements (i.e., minimum size and specificity).
How?

"Consider that there are usually only 20 different amino acids
possible per site for proteins, Eqn. (6) can be used to calculate a
maximum Fit value/protein amino acid site of 4.32 Fits/site. We use
the formula log (20) - H(Xf) to calculate the functional information
at a site specified by the variable Xf such that Xf corresponds to the
aligned amino acids of each sequence with the same molecular function
f. The measured FSC for the whole protein is then calculated as the
summation of that for all aligned sites. The number of Fits quantifies
the degree of algorithmic challenge, in terms of probability, in
achieving needed metabolic function. For example, if we find that the
Ribosomal S12 protein family has a Fit value of 379, we can use the
equations presented thus far to predict that there are about 1e49
different 121-residue sequences that could fall into the Ribsomal S12
family of proteins, resulting in an evolutionary search target of
approximately 1e-106 percent of 121-residue sequence space. In
general, the higher the Fit value, the more functional information is
required to encode the particular function in order to find it in
sequence space. A high Fit value for individual sites within a protein
indicates sites that require a high degree of functional information.
High Fit values may also point to the key structural or binding sites
within the overall 3-D structure. Since the functional uncertainty, as
defined by Eqn. (1) is proportional to the -log of the probability, we
can see that the cost of a linear increase in FSC is an exponential
decrease in probability."

I admit that I don't understand this paragraph. I may attempt to read the whole thing to see if it tells me any more.

http://www.tbiomed.com/content/4/1/47

Overall, the vast majority of potential sequences in sequence space
have no beneficial potential at all at a given level of minimum size
and specificity requirements. You yourself once recognize this as
obvious. I once wrote:
"It seems quite obvious to me that given a particular creature,
such as a bacterium, that the vast majority of possible amino acid
sequences/proteins of a given length will have no beneficial function
for that creature in its current environment."
You responded by saying, "Agreed. This is obvious."
Now I guess it is not so obvious to you any more?
Sure it's obvious. But if you start trying to quantify "vast majority"
you run into problems. Would you not agree that for some values of "vast
majority", random mutation and natural selection would work just fine?

You have to have at least some idea on how to quantify "vast majority"
in order to make this statement at all. What is the basis behind this
statement of yours? How do you know it is the "vast majority" of
sequences in sequence space that would not produce a beneficial
function for a given organism in a given environment? What is the
basis of this statement of yours?

Just a guess, really.

4. And of course proteins aren't random sequences, and nobody says they
arose as random sequences, except in rare cases that are interesting for
that reason. So your model is pointless at its very base.
I've never argued that proteins arose from random sequences given the
existence of the "first living thing". Start with whatever you want
as a pre-established functionally beneficial starting point. My
argument is that regardless of your chosen starting genome, the odds
of adding additional beneficial functional systems to that genome is
exponentially related to the minimum structural threshold requirements
of potentially beneficial systems. The higher the minimum size and/or
sequence specificity requirements of a potentially beneficial system
in sequence space, the exponentially lower the odds that that system
will be within striking distance of your chosen starting-point genome
- - within what anyone would call a reasonable amount of time (i.e., a
few hundred million years).
And Yockey's number has nothing to do with this claim, as far as I can see.

It has a great deal to do with this claim. If the ratio of
potentially beneficial vs. non-beneficial is extremely low even at low
levels, and becomes exponentially lower and lower at higher and higher
levels of FSC (as illustrated by Durston et. al.), you end up with
expanding minimum gap distances that require an exponential increase
in the number of random mutations to cross.

Yes, and Yockey's number has nothing to do with the claim that the ratio of potentially beneficial vs. non-beneficial is extremely low even at low levels. As far as I can see.

Do you think Yockey, Sauer and Olsen pulled their estimates out of
their arses? Hmmmmm?
No, I just think they made estimates using faulty reasoning, which you
have extrapolated way beyond even their data.
Ok - - There's just no reasoning with you. What's the point of
continuing this discussion with someone who demands absolute proofs
before even considering the meaning of available evidence?
I don't recall asking for absolute proofs. I recall pointing out reasons
why you can't use Yockey's numbers for the purpose you intend.
Your reasons are not statistically significant relative to Yockey's
main point - - as noted above.
Only if you pull estimates of their importance out of your nether reasons.

Or consider the statistical and experimental evidence for what it
obviously says - as explained by several mainstream scientists in non-
refuted mainstream literature over the past 30 years.

You argue that the listed authors, to
include Yockey, used "faulty reasoning" to come up with their
published unchallenged peer-reviewed estimates. That's quite a bold
statement given the vacuity of your very strained very unlikely
counter arguments.
That's an argument from authority, right?

If you want to call direct experimental evidence and the conclusion of
scientists who are on your side when it comes to the overall ToE
"authority", then yes.

No, what I call argument from authority is your statement next above.

Evolution is observed all the time, in real time, when it comes to
novel functions that require no more than a few hundred fairly
specified amino acid residues working together at the same time.
There are hundreds if not thousands of such examples published in
literature. Evolution happens even more commonly and rapidly at lower
levels. However, evolution does not happen at all in observable time
beyond the level of a few hundred specified residues. It certainly
has not be observed at all beyond the 1000aa threshold level. There
is a observed exponential decay cure in evolvability that is directly
related to the likely minimum size and/or specificity requirements of
potentially beneficial systems.
This is a version of the old creationist demand to see a cat give birth
to a dog. Genes are duplicated all the time. Sometimes both copies are
retained and gain separate functions. These functions may diverge over
time. What prevents these functions from diverging indefinitely, until
they are different enough to be "novel" by your definition, whatever it is?

I'd hardly call the evolution of a novel 1000aa-based function a "cat
giving birth to a dog". That's a classic evolutionists over
dramatization - a red herring to misdirect; a debating tactic.

It's an analogy. What you are asking for is the protein or genome-level equivalent.

What prevents divergence over time from finding a novel function that
wasn't every in the genome before (beyond the 1000aa threshold level)
are the non-beneficial gaps that prevent the use of natural selection
as a guiding force. Without NS, the time required to find novel
beneficial functional systems at higher and higher levels grows
exponentially with each step up the ladder.

You aren't reading. I'm not talking about any neutral gaps. I'm talking about divergence of function, each step advantageous. Are you saying such divergence isn't possible, or are you saying it can't go very far? Can you, for example, name a single protein family that encompasses different "novel" functions such that it would be vanishingly unlikely to have evolved by known mechanisms?

I don't have enough information to be sure that mutation and selection
are adequate to explain all adaptive evolution, though it does look like
the way to bet at the moment. There can of course be real evolution
without either. As I've pointed out many times, common descent is
evolution, even if God personally zaps every mutation into being, or
zaps multiple mutations at one time to cross your "neutral gaps".
That's a very unusual definition of "evolution". It seems to fit more
with the definition of "slow creation" than with what any mainstream
scientist would call "evolution". Really, such slow creation is not
evolution at all in any standard Darwinian-style sense of the word.
Call it what you like. I would call it theistic evolution, which is a
term invented long ago for just such notions. My main object here is to
determine why you reject that option. So far I have no idea other than
that it doesn't fit your conception of Genesis.

Theistic evolution isn't remotely close to Darwinian-style evolution.
I'm very sure that most in this forum would not back you up with a
suggestion of even the possibility of theistic evolution or what I
would more accurately call "slow creation". Again, I've already
discussion your ideas on theistic evolution extensively. I'm just not
interested in pursuing this topic with you further at this point.

I only wish you would pursue it far enough to actually answer any of my questions. Why do you avoid this so consistently? Here you attempt to distract by objecting to my terminology and suggesting that others may not agree with me. But you never actually address the issue.

If you have no way to test the potential and limitations of NS, it
isn't a science regardless of if you know or don't know of any other
viable alternative.
This is as true for any other theory in science, and as such is a
fundamental rejection of science. I have no way to test whether angels
guide the planets, and so must reject Newton's theory of universal
gravitation as unscientific. Right?

NS is a description of a creative force that is suppose to produce
creative acts in a predictable manner. That should be testable in a
falsifiable manner if it is really a scientific hypothesis/theory.
The same thing is true of Newton's theories of gravity. They make
falsifiable predictions that creative predictive power if they come
true and avoid falsification. You are making a false comparison here
in order to avoid having to actually subject your notions of the
creative power of NS to any sort of falsifiable testing.

I'm not sure how one would test the potential limiations of gravity in your sense. You certainly can't distinguish it from the angel theory. But you seem to be claiming that unless I can re-evolve a bacterial flagellum before your very eyes, the power of natural selection is falsified.

But I'm certainly open to the possibility of other
mechanisms. I see no clear evidence that any other mechanisms are
needed, but there is currently room to postulate them, if you cared to
do so.
The other mechanism, of course, is ID. The same basic argument for
detecting design is used by SETI scientists. Even you use such
arguments behind your design hypotheses for various situations - like
your own scenario of finding a messy kitchen in your house. You said
yourself you would first assume ID in such a situation.
ID isn't a mechanism.

Yes, it is. SETI scientists might not know exactly how an intelligent
agent produce the radiosignal they are looking for (which they would
call "artifactual" if ever discovered), but they would still claim ID
involvement, as a general "mechanism" if such a signal were ever
found.

You need to take that up with SETI scientists.

It's a vague handwave.

Tell that to SETI scientists, forensic scientists, and
archeologists . . .

Tell them yourself. Nobody uses ID as a mechanism. They use the known actions of people.

You have no idea how it
would operate, what sort of evidence it would produce, or how to test
for it.

Sure I do. How many times have I explained the ID-only hypothesis to
you? - the same hypothesis used by SETI scientists, archeologists,
and forensic scientists?

I find the ID-only hypothesis vacuous. Sorry. The people you mention don't use it.

I didn't assume "ID" in the example; I assumed the action of an
entity I know quite well and whose signs I can easily detect.

Semantics. It's the same thing. You can actually hypothesize ID,
quite adequately and reasonably, without actually knowing the entity
directly at all. That, you do understand, is the basic assumption
behind SETI.

I don't understand that.

Again, a belief in evidence for common descent isn't the same thing as
a belief in evidence for Darwinian-style evolution. These are two
somewhat related but still distinctly independent concepts or
theories. Even Behe believes in common descent. Obviously, he
doesn’t believe in Darwinian-style evolution. Are you in the same
camp as Behe? I doubt you would admit it. Yet, you don't really seem
to have any good reason not to be.
I am in the same camp as Behe to a certain extent, as is everyone who
accepts common descent. Unlike Behe, I don't feel I have any evidence
that known mechanisms are insufficient to account for adaptive
evolution, and certainly no evidence that some particular entity is a
viable alternative.

Behe doesn't propose any particular entity as a viable alternative.

Yes he does. He just doesn't want to admit it in some contexts. Behe thinks that god did it, and has admitted this in other contexts.

He, like other IDists, proposes a non-specific intelligent entity.
All he says is that some form of high-level directed deliberate
intelligence had to have been involved in the creation of certain
aspects of living things.

And has presented no evidence for the existence for this phenomenon, whatever that would be.

But what about you? Why do you reject common descent?

I've already told you. . . many many times.

I don't recall that you have. And there's another way to avoid answering a simple question.

I also believe that NS operates in the present. There are an
overwhelming number of examples of its operation. The problem is that
its creative power is demonstrably limited to very very low levels of
functional complexity - relatively speaking. It just doesn't do
anything beyond these low levels and it stalls out, observably, in an
exponential manner at low levels. Statistically these limitations can
be fairly well defined - to a very useful degree of predictive
power.
Beyond this, I have postulated the same hypothesis and basis for this
hypothesis that SETI scientists postulate - the ID-only hypothesis -
to explain functionally complex features that clearly go well beyond
the observable and statistical creative powers of the proposed
Darwinian mechanism.
A nice summary of your claims. But of course you have not shown any such
thing, SETI scientists do nothing like what you have claimed, and you
have not advanced a testable hypothesis.

Please do tell me the basic difference between my basis for suggesting
ID and a SETI scientist's basis for suggesting ID. What's the
fundamental difference as far as you can tell? How can you say that
the ID-only hypothesis is not testable in a falsifiable manner? That
is exactly the same hypothesis that SETI scientists are proposing.
Exactly the same.

We've been over this, and it bores me. Argue with someone else.

You just said that, "I can't be sure that mutation and selection are
adequate to explain all adaptive evolution. . ." Of course, you did
add the disclaimer that, "though it does look like the way to bet at
the moment". That's pretty wishy-washy sounding language if you ask
me. Much more wishy-washy compared to the bravado of those like
Howard Hershy, Okimoto, and many others in this forum and in
mainstream science to be sure.
So you claim.

Where are the problem points, do you
think, for the proposed mechanism that aren't very clear to you?
None in particular. It's just very difficult to find evidence in the far
past for the genetics of a population and the selective environment in
which it found itself. The fairly recent past is not a big problem; for
example, we can determine which parts of the human genome have been
under positive selection in the past few million years. But how to
figure out if the bacterial flagellum was built by selection? I don't
see a way. At most we could come up with plausible scenarios, as Nilsson
and Pelger (1994), for example, did with the vertebrate eye. But coming
up with such a scenario for each and every adaptive change would be a
monumental task.

You call such scenarios "plausible"? - when every single one of their
proposed steps involve vast gaps in non-beneficial genetic changes?

How can you say that? It involves only random phenotypic variance of exactly the sort that regularly exists in living populations. It assumes only that this random variance will be recharged by mutation, which seems a reasonable assumption not requiring descent into any genetic details.

Sure, the morphology doesn't seem like much between these proposed
evolutionary steps, but the underlying genetic changes needed are
absolutely enormous.

What is your evidence or argument for this claim?

This is true for just-so stories of eye
evolution as they are for flagellar evolution - like the best one I
could find proposed by Matzke. How are such scenarios statistically
"plausible"? They simply aren't. Not remotely so.

Why?

Your
position regarding the proposed Darwinian-style mechanism doesn't
really sound all that solid as far as a scientific theory with very
high predictive value if you ask me. I certainly do wonder who else
in this forum might express this same notion in the same or similar
language to that you use here? That would be interesting to know -
for sure ; )
Of course you immediately misconstrue most of what I said, but I'm glad
to provide sustenance for your fantasies if you enjoy that.

How did I misconstrue what you said? Do you see good evidence for the
mechanism of random mutation and function-based selection or do you
just accept it beyond very low levels of functional complexity because
you don't see a decent viable alternative?

I reject all your personal jargon as not meaningful. I see evidence that selection exists. I see evidence that it can move a character indefinitely far from the original population mean, given the right set of changes in environment. I don't know that selection is responsible for huge historical changes (which you deny are changes, but that's your personal problem), but I see nothing inconsistent with that view, and no evidence of an alternative mechanism. You yourself propose no evidence for such a mechanism; at most you show that natural selection is inadequate. The step from that to the idea that intelligence is the only explanation is a large neutral gap indeed.

Accepting something
because you don't see a viable alternative is a much different
position from suggesting that a particular position actually has good
predictive value as a scientific hypothesis much less theory.

Considering that these major changes you don't like happen over immense time scales, what exactly are we going to be predicting? I'm also currently unaware of any way to test for selection farther in the past than comparison with neutral markers can reach. And come to think of it, that's not a test for selection either, because god could have pushed an allele and its hitchhikers to fixation personally, without selection. God makes any test of anything pretty much impossible if you introduce him into science.

.

Relevant Pages

  • Blind Faith in the Mechanism of the ToE
    ... The degree of sequence constraint for such named functions ... varies from protein to protein and within proteins. ... distance or total size of the system. ... named function arose by evolution. ...
    (talk.origins)
  • Re: Most valuable poster
    ... irrelevant mathematical models can't falsify the theory of evolution, ... "functional complexity" is a ratio extracted from a 15-year old paper ... to transform one sequence into another, e.t.c.), and "random walk time" ... The distance between a protein and two of its ...
    (talk.origins)
  • Re: Most valuable poster
    ... understand that denying evolution on *some* level would be lunacy. ... "neutral gap size" is the edit distance ... one sequence into another, e.t.c.), and "random walk time" is one ... The distance between a protein and two of its ...
    (talk.origins)
  • Direct Experimental Evidence for Non-Beneficial Gaps
    ... So we are all agreed that a random sequence of amino acids is very ... The initial proteins would not have such constraints. ... trying to disprove evolution using a static model. ... between the size and sequence flexibility of a protein and Dursten's ...
    (talk.origins)
  • Re: Most valuable poster
    ... nylonase or lactase evolution examples. ... residues), you have the ability, so you say, to tell us *exactly* what ... the average gap size is based on the size of the end product. ... recognizable sequence homologs or recognizable intermediate functions. ...
    (talk.origins)
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