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Sean Pitman  
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 More options Dec 7 2003, 1:19 pm
Newsgroups: talk.origins
From: seanpitnos...@naturalselection.0catch.com (Sean Pitman)
Date: Sun, 7 Dec 2003 18:11:52 +0000 (UTC)
Local: Sun, Dec 7 2003 1:11 pm
Subject: Re: Shakespeare and the Chicken Egg
This is a repaste of a reply to very similar sweetnes comments (linked
below):

sweetnes_n_li...@yahoo.com wrote in message <news:4d71d185.0312060052.2b96f666@posting.google.com>...
> I have presented you with proof (laboratory proof, in many instances)
> that your statements are incorrect.

You have shown that short amino acid sequences can come together to
form a new unified function that is indeed unique and of greater
complexity.  The only problem you have here is that the minimum amino
acid number required for your most complex example is only 3 or 4
hundred amino acids.  My argument is that evolution becomes more and
more difficult the greater the minimum amino acid requirement until it
becomes impossible this side of zillions of years when the minimum
requirement reaches a few thousand amino acids in fairly specified
order.  Where are your examples of evolution requiring such a level of
minimum amino acid specificity?  I see a lot of hot air coming from
you, but no such example.  Where is the reference for such a
demonstration?  And, by the way, your lame bacterial swarming example
doesn't even come close (see discussion below).

Recently I have been referred to the example of the bcr-abl chimeric
protein that causes various forms of leukemia such as chronic
myelogenous leukemia.  The reason for this referral is the fact that
the bcr-abl function is generally realized with the use of between
1000 and 1800 amino acids.  This is good thinking since it is actually
an attempt to controvert my hypothesis whereas you haven't even tried
to present the de novo evolution of anything with a minimum function
requiring over a few hundred amino acids working together at the same
time.

But, before you become excited about the bcr-abl function, there is a
little problem in that it really isn't a new type of function or is it
a selectably beneficial function, but is based on the deregulation of
the pre-established kinase function of the abl protein.  For a more
detailed discussion of bcr-abl function see:

http://groups.google.com/groups?hl=en&lr=&ie=UTF-8&selm=80d0c26f.0312...

> I have provided you with at least three examples of exactly that
> happening: simpler systems combining to produce a novel, complex
> system with a different, novel function. The fact that there are more
> ways to combine systems nonfunctionally does not have a bearing on
> this.

Actually it has everything to do with this.  What you have shown are
simpler systems combining to produce a novel function that requires,
at minimum, only 3 or 4 hundred amino acids.  You have also provided
examples of a simple function requiring less than a few hundred amino
acids at minimum evolving a new type of function within the same level
of complexity, but not anything much greater.  Please, I think you can
at least try and do better than this.

> The system does not work by searching randomly through
> thousands of different combinations of amino-acids, until it "hits"
> the right combination. This has been explained to you over and over
> again. It simply does not happen, and your refutation of this does not
> refute anything that is a part of evolutionary theory.

You haven't explained how my ideas are wrong in this regard.  All you
have shown is how the same type of function can be up-regulated and
down-regulated (See discussion below of Myxococcus xanthus swarming
evolution demonstrated by Gregory J. Velicer and Yuen-tsu N. Yu of the
Max Planck Institute for Developmental Biology) but not how new types
of function within higher levels of complexity can be evolved without
searching randomly through a very large non-beneficial sequence space.
 Sequences with the same types of functions can be clustered around
each other like little islands of stepping stones - very much like a
sentence who's individual letters can be rearranged somewhat without a
complete loss of beneficial meaning, but who's type of meaning is
fairly isolated from other sentences with different types of meaning
or significantly different ways of achieving the same meaning.  How to
cross the non-beneficial gap between these two different types of
meaning?  That is the question?  For shorter sequences, the random
walk required is easier to overcome.  However, with each amino acid
increase in the minimum random walk required to achieve the success of
any new type of beneficial function within that level of functional
complexity, the time required grows exponentially.

> Please show me how would it be possible for a change in biological
> systems, such as it happens NOW, at this moment, to go on for, say,
> ten thousand years, WITHOUT producing a novel, complex system?

Ok - take, for example, a particular function that requires, at
minimum 5,000aa at minimum to be realized.  Say this sequence happens
to get duplicated so that it can undergo various mutations without
risking significant loss to the original beneficial function (which
has been optimized for its host by now - as far as *level* of function
is concerned).  The sequence space at this level of complexity is more
than 10e6500 sequences.  The question is, out of all of these
universes of possibilities, how many are or would be beneficial to the
given organism in question?  If the organism could use a million
different types of functions to some benefit at this level of
complexity and if each of these million different types of functions
had at least 10e1000 different sequences with at least some selectably
advantageous level of function, then there would be 10e1006 total
beneficial sequences in sequence space with a different type of
function.  The question is, how long, on average, would it take to
find any one of these other beneficial sequence islands?  Well, you
have to think of ratios at this point.  What is the ratio of
beneficial vs. non-beneficial sequences in sequence space?  Well,
10e1006 divided by 10e6500 equals 10e5494.  That means that for every
one beneficial sequence there are literally universes of
non-beneficial sequences (i.e., there are only around 10e80 atoms in
the entire known universe).  With a mutation rate of one mutation per
sequences of 5000aa per generation in a population the size of all the
bacteria on earth, it would literally take zillions of years on
average for even one member of the population to find even one
beneficial sequence with a new type of beneficial function at this
level of complexity.

Of course, you will say that evolution doesn't work like this.
Evolution works by getting various fully formed and functional
sequences to get pasted together to gain a new collective function of
higher complexity.  What many don't realize is that the same
statistical problems are involved here.  Finding a way to bring a
bunch of small words or even big words totaling 5000 letters together
where each step is beneficially selectable, is much more difficult
than most people realize.  The same thing is true for functional base
pair or amino acid sequences.  Just because the right sequences are
there as parts of various larger systems of function does not mean
that they will be clipped out and pasted together in just the right
way to make a new system of function that is actually selectably
beneficial at such a high level of functional complexity.

You certainly haven't been able to provide me yet with any such real
time demonstration.  I'm still waiting . . .

> I am only now begining to understand the depth
> of what you are saying. The depth of ignorance in it, that is. I
> didn't understand before that you believe that multiudomain proteins
> are just "as complex as the most complex domain" *literally*. Gods.
> And, to top this, you don't belive in the (slightly more intelligent)
> idea that funcitonalities have to evolve suddenly, in a poof, from
> proteins searching through all possible random combinations; you
> actually believe that long proteins with functions can never arise?!?

A bit of clarification:  I am well aware that many multi-domain
proteins use all or many of their domains at the same time for a
collective function.  However, when you are taking about a particular
function, multiple domains may not be required to achieve this type of
function.  The question is, what is the minimum amino acid part
requirement to achieve a particular type of function to a level where
it becomes selectably advantageous?  I'm not asking how one can make
the most complex Rube Goldberg-type mousetrap here.  I'm asking how
one can make the most simple, bare bones, function of a particular
type that will work to at least some minimal degree of selectable
advantage.  Once you have this function, refining it by increasing or
decreasing its level of function (i.e., more or less lactase ability)
is not a problem.

Now, if you can add to this minimum part requirement to achieve a new
type of function with a higher minimum part requirement (i.e.,
bacterial motility), then you will really have something.  So far, you
have yet to do this.

> There are hundreds of observed instances. Hell, just last week we had
> a seminar on two insect proteins that mutated (independently), and
> formed a complex with third one; the total complex is over five
> thousand residues long. It performs a function totally unrelated to
> any of its three constituents (two constituents are structural
> proteins, one is, of all things, a kinase; new function has to do with
> mitochondrial RNA repair).

Interesting.  Give me the details of this demonstration and/or the
reference for the publication of this demonstration.  Does it involve
the deregulation of the kinase function, as is the case with the
chimeric bcr-able function mentioned above?

> >If such differences really do exist between such
> >otherwise similar creatures, then yes, such systems
> >could not evolve in trillions of years and so they
> >must have been designed.  I cannot comment specifically
> >on the differences between chickens and turkeys, but I
> >can on the differences between several other life forms.

> Such as men and monkeys, eh? Of course.

As I have said over and over again in this forum, I do not think we
know enough about the functional genetic differences between humans
and apes to rule out the possibility of common origin with the use of
genetics alone.

> By your standards, practically every species on earth was designed
> separately and recently. This makes you a YEC. How do you explain away
> the fossil record, the geological data, the radiological evidence,
> cosmological/astronomical evidence, etc?

The definition of "species" is rather subjective.  I do not believe
that all of what are now referred to as "separate species" where
designed separately - although I do believe that they were all here
relatively recently.  The fossil record and geologic data, to include
the radiological evidence, is not nearly as solid in support of the
long ages of deposition that evolutionists claim it is.  It shows very
clear evidence of rapid deposition over the course hundreds and
thousands of years, but certainly not anything even close to a
million, much less a billion years.

See:  www.naturalselection.0catch.com

> >These sequences do not have beneficial functions without
> >the cell being what it is - in other words, it defines
> >such sequences as beneficial based on many other systems
> >of function that recognize and use such short beneficial
> >sequences in a beneficial way.  

> Incorrect. Single amino acids and short polypeptides can (and do)
> catalyze various reactions that could be useful to the proto-organism.

When such sequences are beneficial (which not all of the possibilities
are), they are useful only because the system of the organism
"recognizes" them as useful in a particular environment.  Not all such
sequences, even short sequences, are useful to all organisms. Just
because a particular sequence might be useful in one particular
organism does not mean that all organisms will also recognize it as
beneficial.

> >Try evolving this short word, one letter at a time, into
> >a longer and longer word or phrase. See how far you can go.  

> Quite long, actually. Since words get copied, not just single letters,
> I can get various phrases in.

Try it.  Give a demonstration here.  Provide us with an environment or
situation.  Start with a short word that would be beneficial in such a
situation.  Then, adding letters to that word, evolve it were each
addition makes beneficial sense in that situation.  Spelling does not
have to be exactly correct, just understandable in a beneficial way.
See how far you can go.  Try it here in this forum and include your
demonstration in your reply to this post.

 Plus, proteins are not words.

No, they are not.  They are even a lot more flexible in their
functional sequencing.  But they are very similar in that they are not
completely flexible in their functional sequencing.  There is a
minimum limit to the size and order required by a protein-based
function - beyond which all beneficial function suddenly ceases.  This
characteristic creates the neutral gap problem just like it does for
English words, sentences, and paragraphs.

> >Again, a multi-domain protein is no more complex in
> >functional ability than its most complex functional domain.  
> >The functional domains work independently.  It is like multiple
> >proteins stuck together.  But, these domains do not necessarily
> >work at the same time to give a greater unified function.  

> This is perhaps the best example of how poorly you understand
> biochemistry. Considering that your pet lactase is a multidomain
> protein, I wonder how I didn't catch on to this earlier (I know why,
> actually: I gave you far too much credit, and couldn't believe that
> you would claim what you claim without knowing at least some basic
> things).

You will notice that I use the word, "necessarily".  A many types of
protein functions do not necessarily require multiple domains in order
to be realized.  You yourself admitted as much in your first post when
you claimed that the lactase function is actually much simpler than
its usual 1000 acids would make it appear.

> Practically every large protein is formed of multiple domains, which
> ALL work TOGETHER to produce the function of the protein.

Certainly this is true.  If you can present the evolution of such a
collective function that requires, at minimum, all of the various
amino acids in all of the various domains of a particular protein
working at the same time, then you will have something.  You have
tried to do this, but your total number of specified amino acids falls
rather short - being less than 500aa so far.  You claim to know of
functions that require much more than this, but you have yet to
provide me with the details of such observations and/or a reference to
support such claims.

> One domain
> recognizes the substrate, another may carry the active site of
> catalysis, the third may be involved in carrying the product (or
> recognizing and binding a coenzyme or second substrate...). If you
> don't have specifically defined domains, you have so-called motifs,
> which are smaller sub-domain like structures.

Yes - I agree and know full well about such collective functions. I
think you have misinterpreted what I was trying to say.

> Large proteins that do not work like this are *extremely* rare (which
> is to be expected).

Certainly . . .

> >Beyond a few hundred amino acids required at minimum, such
> >functions simply do not evolve.  

> I gave you examples of them evolving.

Where?  You made a blanket statement but you provided no details or
references to support this statement.

> Sean. I am a biochemist. I work with this stuff every day. How stupid
> do you think I am? You are trying to teach me how to do my job, and
> you are not very good at it.

I don't think you are stupid and I do not assume to teach you how to
do your job.  However, I highly doubt that your job invokes the use of
evolution beyond the lowest levels of functional complexity.  You
claim that it does or that you do in fact observe such levels of
evolution all the time, but you have yet to support such claims beyond
those that require more than a few hundred amino acids.  What I am
talking about here are those types of beneficial functions that
require, at minimum, several thousand amino acids working together at
the same time in a rather specified order.

> Novel proteins of sizes measured in thousands of kD have arisen
> through evolution, in laboratory conditions.

References?

> Well, since the examples I gave you so far simply don't
> count for some reason (mostly that you refuse to accept that things
> happen if your theory says they cannot happen), let me give you a
> relatively recent one. Velicer and Yu, at Max Planck institute in
> Germany; the bacteria, under pressure, developed a complex
> etracellular fibril matrix, and adapted it to achieve a form of
> primitive cooperation.

Actually the M. xanthus bacteria did not develop their extracellular
matrix de novo.  They were in fact already able to make this matrix
via the use of pre-existent genes.  What happened is that when Velicer
and Yu deleated the genes that gave these bacteria that ability to
achieve S-type swarming, they increased their ability to make more
matrix necessary for A-type swarming.  What they evolved was the
ability to make "enhanced quantities" of a matrix which they already
made. In fact, genetic mutants of the evolved strains were constructed
by Velicer and Yu that were unable to make this fibrilar matrix even a
little bit, and guess what, these bacteria never could evolve any type
of significant swarming ability, much less the A-type or S-types.
"Both the genetic and chemical inhibition of fibril-matrix
construction inhibited the evolved swarming phenotypes."

http://www.eurekalert.org/pub_releases/2003-09/m-wsb090503.php

Basically, this is no different than the evolution of penicillin
resistance in bacteria who already have the gene for penicillinase and
all they need to do is make more penicillinase enzyme by decreasing
suppression of penicillinase production.  The evolution of decreased
suppression of production of a fairly complex enzyme like
penicillinase is not nearly as difficult as is the evolution of the
penicillinase code to begin with.  A single point mutation (many
different ones) can decrease suppression of production.  The same
thing happened with this case of M. xanthus swarming evolution.

Please!  You really should try to do better than this!  I really
thought that you might have it more together - being a "biochemist"
and all.  Come on now, is this the very best that you have to offer?
Perhaps you don't like to list the actual references to research
studies like this because you know how very limited they are and that
they really do not support your contentions and most exaggerated
statements in the least.

In any case, this is all the nonsense I have time for today.  Hope you
come up with something much better by Monday - as promised.  Good luck
. . .

> M.

Sean
www.naturalselection.0catch.com

 
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