How does evolution really work?

Sean Pitman M.D.

This is an interesting exchange I had in an origins debate forum called Talk.Origins(Google.com). It concerns the mechanism, or lack thereof, for Darwinian evolution. I hope you find it interesting. (My comments are in green and black while John Harshman’s are in purple).

> > 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

> plastic”.)

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

3D shape/structure.

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

given environment.

> > 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

nonfunction.

> 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.

> I’m

> 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

> enough.

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

naturalistic process.

> > 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

differences then?

> > 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

detected.

> 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

fails.

> > 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

functional hand.

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

out there.

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?

Sean

www.DetectingDesign.com