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's are in
purple).
John Harshman
> > 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.naturalselection.0catch.com
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