> > 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.
> Agreed. This is obvious.
> > Only a very tiny
> > fraction of the potential amino acid sequences will be recognized by
> > any given bacterium or living cell in any given creature.
> Recognized? What meaning are you using for "recognized"?
Take for example the insulin protein. Not every cell in the body
"recognizes" the insulin amino acid sequence. Other cells, having the
proper surface receptors, do recognize the insulin protein and perform
various functions when insulin comes around. So, for some cells the
insulin protein really has no function or meaning while for other
cells it does. It is like different words for different languages. A
given word might have some meaning in Spanish, but none in English.
The same is true for protein "words" in living cells. A given
protein/amino acid sequence might have function or "recognition" for
one cell, but have no function/meaning/recognition for another cell.
If a given part performs some sort of function in a given system of
functional parts, then that part is "recognized" by that particular
system. The system "knows" what to do with that part. It "knows"
what function that part has. For example, the term "recognition" is
often used when describing the interactions of antibodies with
antigens. When the antibody comes in contact with a particular
antigen that it fits with, the antibody is said to "recognize" the
antigen. Does this make sense now?
> > Take humans
> > for example. The vast majority of human DNA does not code for any
> > functional protein much less a beneficially functional protein. The
> > proteins that are coded for are somewhat plastic, true, but they are
> > also very specific. If changed or "denatured" to any significant
> > degree, they loose all function.
> You are confusing two forms of change. We were talking about mutation.
> Denaturing is a loss of tertiary or quaternary structure, most often as
> a result of heating. Nothing to do with what we are referring to. (Also,
> I don't understand your distinction between "functional" and
> "beneficially functional", or what you mean by "somewhat
I mention protein "denaturing" to emphasize the idea that changes in
protein sequence *and* structure affect protein function. We are
talking about protein function in general here. Whatever changes a
protein (mutation, heat, chemicals etc) can affect its function in a
given system of function since protein function is dependent upon its
Also, a protein can be functional without being "beneficially"
functional. For example, a protein can have a "detrimental" function.
> > This means that the vast majority of
> > potential protein sequences and three-dimensional shapes are worthless
> > to a given human cell.
> This is not quite clear, at least the "vast majority" part. There are
> lots of protein sequences that don't do exactly what we would like, but
> it does appear that we can find function from random sequences. See
> this: Hayashi, Y., H. Sakata, Y. Makino, I. Urabe, and T. Yomo. 2003.
> Can an artibrary sequence evolve towards acquiring a biological
> function? J. Mol. Evol. 56:162-168.
Of course one would expect that various random sequences could be
found that do actually have some sort of function in a given cellular
system of function. Some of these might even have a "beneficial"
function in a given cell and environment. However, the vast majority
of potential sequences of a given length and 3D structure will not
have a function at all. You admitted as much above. When I said, "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 said, "Agreed. This
is obvious." Well then, what are you trying to do here? You seem to
be contradicting yourself in the same breath.
I see it much like a language system of function. Pick a given
sequence length of words. Lets pick a sequence length of 3-letter
words. How many 3-letter words are defined by the English language
system? Quite a few, but probably not 17,576 which is the total
number of possible 3-letter words. Surely there is a sizable
percentage of defined 3-letter words as compared to the total possible
number of 3-letter words... true. Therefore, it is relatively easy to
change a letter in a 3-letter word and get to a new functional word
such as the evolution of "cat to hat to bat to bad to bid to did to
dig to dog." However, will this work so easily when we are talking
about say, 6-letter words? There are 308,915,776 different 6-letter
sequences or potential 6-letter words out there. Relative to this
number, the number of defined or "functional" 6-letter words in the
English language system of function, are few. It is much more
difficult to "randomly" pick out of this pile of 6-letter words a word
that will have some sort of function or "recognition" when spoken in
an English speaking crowd.
So yes, one would expect that there would be "lots of protein
sequences" that could be picked at random out of a mix of protein
"words" that would have some function for a given cell in a given
environment. However, I am willing to bet that these functions are
usually quite simple, having to do with enzymatic activities that
require relatively short amino acid sequences to perform them (like
3-letter words). Such functional sequences would be found to be
relatively common in a random mix of proteins. However, when one
starts increasing the complexity, the difficulty for picking a protein
with a function of higher complexity becomes more and more difficult
(As with the challenge of picking, at random, a functional 6-letter
word from a mix of 6-letter sequences). It might not be "impossible"
to randomly pick such a sequence, but it would take a lot longer time
to be successful on average.
The average time involved becomes the problem because, with increasing
complexity, the total number of sequences with potential function
decreases dramatically leaving larger and still larger gaps in
function between those sequences that would actually have function for
a given cell in a given environment. The random drift or "selection"
involved in getting from one sequence with function to any other
sequence with a different function of comparable complexity requires
greater and still greater amounts of time.
> And the introduction of 3-D shapes only confuses the question.
Actually, the 2-D sequence of proteins really is not what does the
job. The 3D structure is what really matters when it comes to protein
function. The same sequence can be folded in different ways. And,
depending upon which way the protein is folded; function may be gained
or lost. Proteins do not always spontaneously fold in the proper way
to realize their function. There are other proteins that fold new
proteins as they are made. If the 3D structure of a particular
protein is "unfolded" and then allowed to "refold" by itself, it most
likely will not fold properly and its function will be lost. So,
really, we talk about the 2D sequence because it is easier to talk
about, but in reality, the 3D structure is very important to function
and only compounds the problem of complexity since even more
differences can be realized for a given amino acid sequence than a
simple 2D sequence analysis would suggest. For a 2D sequence of 10
amino acids, the total number of potential proteins is:
10,240,000,000,000 (~10 trillion). However, the total number of
different proteins would actually be much higher than this because of
all the added differences in 3D structures that are not being included
in the total number. This makes for even less of a chance of picking
those sequences/3D structures of amino acids that actually have some
sort of function, much less beneficial function, for a given cell in a
> > As far as demonstrating a negative (ie: A lack of a functional path
> > between two different proteins), it is impossible this side of
> > eternity. A negative finding never means that a positive finding is
> > impossible. However, the likelihood that a negative finding will
> > occur can be calculated.
> If it can, then you haven't done it yet. This remains to be seen.
Well, of course I disagree. Can you prove that these gaps do not
exist or explain how they might not exist? For example, can you show
how a relatively complex function, such a bacterial motility (Any
type, not necessarily flagellar motility), could evolve where no
genetic gaps in function would need to be crossed? There are those
who suggest that there is no goal in evolution. Therefore, the
testing of a specific "goal" such as the evolution of a specific
function, such as motility, is not a valid challenge of evolution
since a given type of bacteria may evolve other equally complex
functions before motility is ever evolved.
This is a great argument. For one thing, without a goal to defend,
there is no need to move goal posts as YECs are so often accused of
doing. Just because a particular function does not evolve, such as
the lactase function in certain of Hall's bacteria, does not mean that
evolution is having problems. It only means that evolution does not
need to travel down any particular path, regardless of the benefits
that would be realized if that path was traversed. Well, Ok... lets
go there. Naturalistic evolution obviously does not "know" which path
to choose. It can go down any path in any direction and eventually
get somewhere with some beneficial function. Sure it can. However,
what if each starting point is completely surrounded by a huge ocean
of neutral function or nonfunction? Consider that if there were 1
million defined 6-letter words that each word would, on average, be
surrounded by 300 non-defined words. No matter which way evolution
went, odds are that it would quickly run into a gap of nonfunction
that separates current function from new function. Try it. Starting
with a 6-letter word, how far can you go before you are blocked by a
gap of nonfunction? Now, if that seems hard, try to evolve a larger
sequence of letters, such as a sentence of words, one letter at a time
and see how far you can go before you are blocked by sequences of
> How do you
> know there are such gaps? For eyesight, it has certainly been shown that
> there is a continuous series of slight morphological variants, each
> advantageous, from a patch of light-sensitive cells to a camera eye.
A series of morphologic variants that appear to follow a smooth
evolution of very small steps is deceptive in that is covers up the
complexity of the genetics involved. If in fact every "slight"
morphologic variant was the result of an equivalently "slight" change
in the genetic code then you would be correct in your statement that
such a series of morphologic variants give convincing evidence of
common descent. However, there are several problems with such an
automatic assumption. One problem is that apparently small
morphologic changes often require relatively large changes in the
underlying genetic code. The same is true for computer functions.
Apparently "simple" or "small" changes in a program's function often
require comparably large changes in the underlying code. For example,
going from a "simple" eye spot or collection of light sensitive cells
to a slightly concave eye cavity spot, seems morphologically simple,
but the genetics involved are quite complex. All the cells involved in
the formation of this cavity must be programmed to relate with the
other cells in this area in a very specific way to form this
concavity. This orchestration requires many very specific genetic
changes. Gaps in beneficial function are certainly involved. Another
problem is that function is arbitrarily attached to code. Very
different codes can and do code for the same or similar functions and
very similar codes can and do code for very different functions.
Because of this arbitrary nature of code, a change in the code will
probably not result in an equivalent change in code function or
"morphology". Very small changes in code can result in huge changes
in morphology. Also, very large changes in code might not change
morphology/function very much at all.
An argument based on morphology alone might seem compelling if that is
all that one had, but we know more now than Darwin knew. We know that
there is an underlying code or genotype that gives rise to morphology
or phenotype. If you can explain, genetically, how the gaps between
these various "small" differences in morphology can be explained, then
you would certainly win the Nobel Prize. As of yet, I have found no
detailed genetic explanation or real-time experiment that explains or
demonstrates how the evolution of morphologic variants, such as the
morphologic eye variants or various bacterial motility systems,
evolved or even could have evolved.
> sure you are familiar with How would one go about demonstrating that
> there are or are not such gaps with respect to feathers?
Yes, try to evolve a feather or a feather-like structure or to
estimate how long it would take based on genetic sequence analysis,
mutations rates, functional genetic intermediates, and the length of
the average genetic pathway to such a function in a given creature.
Detail the genetic codes involved in coding for feathers and then
compare these codes to the codes that are available in other
non-feathered creatures and see if a genetic path could be detailed
and how long it would take to cross this path.
> We do know that
> feathers arose in a bipedal, non-flying dinosaur. That seems clear
Oh really? How so? Is there a gradual step-by-step demonstration of
this evolution in the fossil record? Not any more than could be
detailed various creatures all living at the same time today. It is
the same argument as the evolution of simple to complex eyes. Get a
bunch of different kinds of eyes and line them up in a morphologic
sequence from more "simple" to more "complex". Obviously, once this
lineup is complete, the conclusion must follow that the simple eyes
gave rise to the more complex eyes. This might seem reasonable at
first glance, but this is not necessarily a correct conclusion.
Practically any collection of objects can be categorized in such a
manner, but this does not mean that these various object arose via
common descent... especially if the mechanism to adequately explain
such variations is weak. For example, the various books on my
bookshelf can be categorized in this manner, and just as convincingly,
from more "simple" to more "complex." But, this does not mean that
the more complex books arose via common descent from the less complex
books even if the changes between them seem to be relatively small.
You see, without an ability to detail a mechanism of change, the
differences and similarities, by themselves, do not necessarily
support the position of common descent.
> Whether they arose by natural selection, or by any naturalistic
> pathway, is difficult to determine. I suppose you could, if you liked,
> support some kind of theistic evolution in which God gives the
> occasional nudge to get a genome across some functional gap. I'm not
> sure where you would find evidence for it, as there is for selection,
> and I'm pretty sure you would reject such a theory anyway. Right?
The evidence that you have is one of morphology alone, not of
genetics. The morphologic evidence is not compelling enough to
adequately support the theory of common descent. You need genetic
evidence or some way to explain how the genetic gaps can be crossed.
Also, I find the standard interpretation of fossils and the geologic
column unconvincing and quite biased or colored by the a priori
assumptions of evolution and naturalism. I see no clear evidence that
feathers must have evolved from featherless creatures. The fossil
record is a static record and is thus quite limited in what it can
tell us about the lives and changes of creatures over time. You need
real-time examples detailing the actual genetic changes in life forms.
Relying on morphology is easy to do, but it is rather weak when it
comes to explaining how the genetic codes themselves evolved via some
> > If you think that a neutral gap in function
> > that requires just one protein sequence is hard to cross, try crossing
> > a gap that requires the evolution of multiple proteins to cross where
> > hundreds or even many thousands of neutral mutations are needed.
> I agree that this scenario sounds unlikely. I just don't agree that it
> is necessary.
Why not? What *genetic* explanation do you have to account for the
> > If there were such a path from scales to feathers, then we should be
> > able to quickly demonstrate such evolution in real time.
> I deny that there is any such expectation. Why should there be? Are you
> saying that we should be able to demonstrate every possible occurrence
> in the lab? Why? If we are talking about something that took millions of
> years, why should we be able to do it in one or two? And this assumes
> that we know what steps are necessary, which we don't, at least not yet.
If it took millions of years... why did it take so long if there was a
beneficially functional path each step (mutation) of the way?
> You have the kernel of an interesting point there, and it's been a
> conundrum of evolution for some time. Why is evolution so slow over the
> long term, when natural selection is so fast? I think there are several
> reasons: waiting for mutations, waiting for the environment (internal
> and external) to change so that new selective pressures are seen, and
> following a twisty path around constraints rather than the straight path
> you seem to think is the only possible one. It's an interesting problem,
> but not as you seem to think a disproof of the efficacy of selection.
Mutations occur quite rapidly. For humans, the average mutation rate
is around 250 mutations per individual per generation. In a large
population, such mutations, if a fair proportion were directed in some
way, would result in rapid evolution along a great variety of
evolutionary paths. Feathers, wings, eyes, legs, arms, and a host of
potentially beneficial functions would evolve in short order. The
problem is that the path is quite "twisty" indeed. The path is not
straight. That is the problem. The path is very curvy because of the
random drift problem. If each and every step is not selectively
advantageous, then evolution starts to wander around a neutral sea of
function. The wandering is very curvy or nonlinear. In fact, it is
such a curvy path that millions, billions, and trillions upon
trillions of years are simply not enough to traverse this path. The
"efficacy of selection" is dependent upon nature's ability to select
between different genetic changes. If the changes are "neutral" in
function then natural cannot select between different genetic
sequences that have the same function (or nonfunction). At this point
the "efficacy" of natural selection is severely limited.
> > There are gaps between various functions that
> > require a lot of time to cross. In fact, many of these gaps seem so
> > wide that billions or even many trillions upon trillions of years are
> > simply not enough.
> If there are, name one and show the evidence that it is such a gap.
I already have. Depending on the complexity of the function in
question, the evidence for non-evolution can be found in comparing
what is available with what is needed. The lactase function in E.
coli is a good example of this non-evolution. When lacZ and ebg genes
are deleted from E. coli, they simply do not use any other genetic
sequence to evolve the lactase function despite being observed for
many thousands of generations while growing on selective media that
would benefit them if they were ever to evolve the lactase function
again. B. G. Hall himself described such E. coli colonies as having,
"limited evolutionary potential." Obviously these limits are there
and they are found in the form of neutral/nonfunctional genetic gaps
in function. All codes/language systems have these gaps. Human
languages, computer languages, and even genetic languages/codes have
these gaps. Natural selection cannot cross gaps in function in any
directed way. Without direction, mutations are purely random and
random changes wander around a very curvy path that simply takes to
long to come across new beneficial functions.
> > You know that naturalism is
> > the answer... without knowing how it works?
> Did I mention naturalism? No. In fact I mentioned divine intervention as
> one potential mechanism. So your comments are irrelevant. I'm talking
> about common descent. Would you care to argue about the evidence for
> common descent?
The theory of common descent is a naturalistic theory. It is an
argument from the position that nature and naturalistic processes can
explain the variety in living forms. You are therefore "mentioning
naturalism." You mentioned "divine intervention as one potential
mechanism" but you do not believe that this is the mechanism over the
idea that a naturalistic process is a more likely or reasonable
explanation. For myself, I'm not so much arguing for the identity of
the designer as I am for the fact that there is evidence of design,
from some intelligent source somewhere, in living things. Humans are
also capable of such designs in code and systems of function. Are we
therefore "divine"? No, but we certainly are capable of
"supernatural" activities in the sense that non-intelligent natural
processes, such as random mutation and natural selection, are
incapable of performing. A tree limb, as it is blown by the wind, may
break a window without relying on deliberate design or creative
intelligence. However, there is no naturalistic process for fixing
the window and putting it back in its place outside of deliberate
design/creative intelligence... regardless of where this intelligence
came from... be it divine or human or an intelligent alien from the
planet Zorg. Whatever the source of intelligence, the fact that
"supernatural" intelligence (ie: above the naturalistic
non-intelligent processes of a mindless nature) was required can be
> I didn't mention anything about random mutations. I'm talking about
> common descent. Common descent is separable from the mechanism that
> causes adaptation. You, as a creationist, deny common descent. I'm
> saying that if, somehow, you were to show that natural selection is
> insufficient as a driving mechanism, then the evidence for common
> descent would remain untouched and conclusive.
Not so. Without a knowledge of the mechanism of common descent, the
evidence for common descent is far from "conclusive." Common descent
is not a forgone conclusion, especially if the mechanistic explanation
> > You obviously have a very great faith in the power of naturalism to
> > answer all questions pertaining to the physical universe. For you,
> > the very notion that there just might be evidence of design in the
> > natural world/universe is simply out of the question.
> I said nothing whatsoever either for or against design. I'm not talking
> about design. I'm talking about common descent. Is that clear?
When you are arguing in favor of common descent, you are arguing
against design. The theory of common descent is a theory that tries
to propose a naturalistic cause, outside of design, to the existence
of various life forms. So, really, you are talking about design.
Whether or not you admit it or realize it is another issue.
>I happen to believe, based on the evidence,
> that natural selection is a pretty good mechanism and that evolution has
> indeed proceeded "naturally" (and there is considerable evidence that
> evolution has no particular goal), but that's not at all what I'm
> talking about here. Your inability to separate "darwinism" into
> independent components is causing a communication failure.
You would like to think that one component has no bearing on the other
components of the theory, but the fact of the matter is that all the
components of Darwinism are intimately intertwined. If one basic
component fails, the whole thing fails. I suppose you could say that
the theory of evolution is... "irreducibly complex." ; )
> Actually, under normal conditions most mutations occur during DNA
> replication, which I believe does occur simultaneously with cell
> division in most prokaryotes.
Yes, this is true. However, these mutations, once they occur, are
passed on from one generation to the next.
> > However, once the mutations occur, these mutations
> > are passed on to the bacterium's clonal offspring via the
> > division/replication/mitotic process.
> Mitosis is something that happens in eukaryotes, not prokaryotes.
True again, but prokaryotic replication/division/fission is similar to
eukaryotic mitosis. The offspring are "clonal" in both cases.
> Once again: hypermutations are observed to occur in bacteria that are
> not actively dividing. Generally they happen under starvation conditions
> in which the bacteria cannot reproduce. If one bacterium experiences a
> mutation that lets it reproduce, then the subsequent colony descends
> from that one. Actively dividing bacteria do not experience these
> hypermutational rates.
True again. However, in my calculations I wanted to raise the
mutation rate as much as possible in favor of the evolution of new
traits in a reasonable amount of time. Hall also used other mutagens
to increase the mutation rate in his colonies. In any case, the point
of the high mutation rate is to show the difficulty in crossing
apparently small gaps in function.
> > In fact, Hall
> > does so in his own paper. He makes his own estimations of the
> > mutation rates for his bacterial colonies, "per generation."
> Are these hypermutational rates, i.e. a response to stress? I'm afraid I
> don't have the paper available in front of me.
The mutation rates that I used in my calculations are higher than
those used by Hall in his calculations. The mutation rates that he
uses are increased over normal because he used various mutagens to
increase the mutational diversity in his experiments.
> Every analogy is imperfect, but I think we can get a little more out of
> this one. Let's define a "non-functional" bridge hand as one with less
> than 13 points, and a "functional" one as having 13 points or more. If
> this is so, then even though there are many more nonfunctional than
> functional hands, and even though any given functional hand is
> vanishingly rare, still there are enough functional hands dealt to keep
> a game going. So with life. We are not picking a fixed target and
> attempting to approach it with mutations. There are many possible goals
> and many paths to each one. Even if most changes lead nowhere, it's
> enough that some changes lead somewhere.
Given 52 different cards in a deck and 5 cards in a hand, there would
be 380,204,032 different possible hands. If only 1 million hands had
a "function" what would the odds be that a "functional" hand would be
drawn any given round? 1 in 380 tries... right? If each try takes 10
minutes, the average time needed to draw a functional hand would be
~2.5 days. You see, each functional hand, on average, would be
separated from every other functional hand by a relatively small sea
of nonfunctional hands. Still though, no matter which direction you
would happen to go, the odds are that you would end up with many
nonfunctional hands before you would come across *any* other
As you said, "So it is with life. We are not picking a fixed target
and attempting to approach it with mutations. There are many possible
goals and many paths to each one." The problem is that every path is
long no matter which path is taken. In fact, when it comes to certain
complex functions in living things, the average distance of a path to
any one of a number of possible goals is so large that even with a
huge population taking many different paths, the time required to
reach any of the potentially beneficial targets is still huge. For
example, take those functions that require at least 100 amino acids to
perform them. How many of these functions would be beneficial to a
given organism in a particular environment? Maybe a billion? or a
trillion? Maybe a trillion trillion? Maybe, but most likely not
anywhere near the 1 x 10e130 different potential 2D sequences that
could be had. By far the vast majority of these 1 x 10e130 proteins
would be of no beneficial use to any particular organism. If even a
trillion trillion functions could be of some beneficial use, this is
still a tiny fraction of the total leaving only slightly less than 1 x
10e130 different proteins that would not be beneficially functional.
This means that each one of the trillion trillion functions would be
surrounded by 1 x 10e106 proteins that would not be beneficially
functional. In moving from one function to any one of the other
trillion trillion functional sequences out there, one would have to
cross a vast sea of nonfunction... no matter which direction one
started out in. These functions are like tiny islands in a vast sea.
No matter how many beneficial functional islands there might be out
there somewhere in this ocean, the waters of nonfunction that separate
them are vast indeed. The boat of neutral evolution just drifts
around on this sea randomly until it comes across some new function
that can be recognized as beneficial by natural selection. However,
until this new function is realized, natural selection is blind to all
neutral/nonfunctional genetic changes that occur in the meantime.
This leaves random chance as the loan power for change. And, random
chance alone simply takes too long to cross this sea to any one of the
billions, trillions or even zillions of possible functions that may be
It is like a lottery where there are a million winning numbers. It
seems like a cinch to win by picking at least one of so many winning
numbers until one realizes that for every winning number there are a
zillion loosing numbers. How long, on average, will it take to come
across any one of the one million winning numbers if there are
trillions upon trillions of loosing numbers for each winning number?
You see, the deck is heavily stacked in favor of loosing when it comes
to the realization of any sort of complex function that requires the
crossing of even a relatively short gap of neutral change.
> > To
> > get to a new function requires random neutral drift around a huge sea
> > of neutral/non-functional sequences.
> You assume this but there is no reason to suppose it, and no reason to
> suppose a single target as all your calculations assume.
There is plenty of reason to "suppose" this. You yourself admitted
that there are most likely far more nonfunctional sequences than
functional sequences. My calculations use a single function as an
example, but I need not assume a single target at all. Even given
millions of potential targets, the problem remains that each one of
these targets is still surrounded by a huge sea of nonfunction. The
Bridge Game analogy is very good in this regard, but it is limited in
that the odds in favor of getting a functional hand, within your
definition of function, are still pretty good because of the limited
nature of each hand of bridge. However, when you expand the hands to
compare with the size and complexity certain genetic functions, the
odds get much much worse. Instead of having a hand of only a few
cards, try using a hand of 1,000+ cards while only having a few
million winning hands out there.
> > In the replacement of a particular base in a sequence of DNA, the
> > replacement could replace the base at the position in question with
> > the same base 1/4th of the time. Therefore, the odds that a given
> > "change" will result in a specific base are 1 in 4.
> If a base is replaced with the same base we don't call it a mutation. We
> don't call it anything, except maybe "replication". A mutation rate that
> includes "no change" would be a rate of 1 per site per generation, since
> every site will either change or not change. You really need to fix this.
Ok... I've thought about this point further and you've got me here. I
will fix this. Thanks for pointing out this error, but it really has
no significant bearing on the point at hand. Be the odds 1 in 4 or 1
in 3 makes no real difference as far as the problem is concerned.
> Well, it [neutral evolution] does say how neutral gaps can be crossed. With low probability,
> getting lower as the size of the gap increases. If there is a large
> neutral gap between two functional proteins it is unlikely to be
> crossed. But who says that such gaps are prevalent?
You are one of the more reasonable evolutionists that I have come
across. At least you recognize the problem and seek a reasonable
solution, such as the idea that such gaps do not exist. If such gaps
really did not exist, then yes, evolution would not present a problem
at all. However, it seems like you understand that if such gaps do
exist that they would actually present a significant problem for your
theory. You see that a gap crossing of low probability requires more
time to be overcome and that this time increases with the size of the
neutral gap. But, you believe in evolution so much, based on other
evidences, that such gaps really must not actually be there. They
might be there for certain targeted functions in certain narrow
situations, but certainly not for all functions. You propose that
there are so many potentially beneficial functions out there that all
the various paths that might be taken are bound to come across at
least a few of them in a reasonable amount of time, even if they be
quite complex... such as bacterial motility or camera-like eyesight.
Well, let me turn the tables here and ask you to defend this
hypothesis of yours. Upon what basis do you propose that these gaps
do not exist? You obviously "agree" that the vast majority of
possible amino acid sequences of a given length would have no
beneficial function for a particular organism in a particular
environment. Given this agreement, how do you propose that no gaps
exist between functional sequences? Are they all clustered together
like a bunch of islands in an archipelago? Even the "functional
hands" in your hypothetical game of bridge are each separated from
each other by many nonfunctional hands. These are "gaps" in function
between functional hands of bridge. Since these gaps exist in your
hypothetical example, how then can you propose that they do not exist
in the genetic cards/deck of a given gene pool? Please, upon what
evidence do you propose the absence of significant gaps between
various genetic functions as these functions move up the continuum
from more simple to more complex?
. Home Page . Truth, the Scientific Method, and Evolution
. Maquiziliducks - The Language of Evolution . Defining Evolution
. DNA Mutation Rates . Donkeys, Horses, Mules and Evolution
. Amino Acid Racemization Dating . The Steppingstone Problem
. Harlen Bretz . Milankovitch
Since June 1, 2002
Stacking the Deck
God of the Gaps
The Density of Beneficial Functions
All Functions are Irreducibly Complex
Ladder of Complexity
Chaos and Complexity
Confusing Chaos with Complexity
Scientific Theory of Intelligent Design
A Circle Within a Circle
Mindless vs. Mindful
Single Protein Functions
BCR/ABL Chimeric Protein
The Limits of Functional Flexibility
Functions based on Deregulation
The Geologic Column
Matters of Faith
Evidence of Things Unseen
The Two Impossible Options
Links to Design, Creation, and Evolution Websites
Since June 1, 2002