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