Re: Ron Okimoto and the Gap Problem

On Sep 4, 10:12 pm, "R. Baldwin" <res0k...@xxxxxxxxxxxxxxxxxxxx>
wrote:
"Seanpit" <seanpitnos...@xxxxxxxxxxxxxxxxxxxxxxxxxxx> wrote in message

news:1188890449.317203.108110@xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

On Sep 3, 7:42 pm, "R. Baldwin" <res0k...@xxxxxxxxxxxxxxxxxxxx> wrote:

A biological system that is does not produce some sort of beneficial
function will not be in existence for very long. It will be lost
because nature will not select to maintain it. Those that remain in
the gene pool remain because the produce some sort of reproductive
advantage. Different types of potentially beneficial systems have
different minimum structural requirements without which they cannot be
realized in the gene pool at all.

I can see no reason that a neutral bit of tissue must be selected
against.

It cost energy to maintain DNA. Therefore, DNA that isn't providing
any benefit to the creature will eventually be discarded.

There seems to be an awful lot of wasteful, do-nothing, layabout DNA in most
organisms. Why is that?

Well, for most eucaryotic organisms and, in particular, multicellular
or large eucaryotes with relatively slow reproductive rates.
Parsimony in DNA appears to be correlated with small size,
unicellularity, and rapid reproduction, as occurs in yeasts and
bacteria. For fat, lazy, slow-growing eucaryotes like humans, the
amount of DNA per cell is not correlated strongly enough with
reproductive success (the only measure that counts) to be a
significant factor. It is also possible that larger amounts of DNA is
one easy way to increase cell size via a feed-back mechanism that
regulates cell size to nuclear size (plant breeders take advantage of
this; most commercial, i.e., big, flowers are polyploid) which has
possible advantages in certain lifestyles or niches. In that case,
carrying a load of otherwise useless "junk" DNA might have some
advantage, but that would NOT be a sequence-dependent use of DNA.
Some 95+% of human DNA is sequence-irrelevant material, to give a more
accurate definition of "junk DNA", of course.

Besides,
this discussion is about the time it takes to find useful genetic
elements with different minimum size and specificity requirements.

I don't accept your bald assertion that there is such a thing as minimum
size and specificity. I'm not alone in this. You need to demonstrate it, if
you want anyone to accept your arguments.

And Sean needs to explain how *he* thinks different genes arise (what
natural method -- since only natural methods have natural effects --
was used), when they arose, why they exhibit the pattern of
differences (for a given function) that they do, *and* present the
*material* evidence that this is what actually happened to produce
these results.

We have given him the mechanisms (duplication and divergence, chimera
formation, various forms of mutation), mechanisms that are *actually
known* to occur in nature, that can produce the modified or novel
functions that *have* evolved. We have demonstrated that, given
standard times since divergence of currently living groups from common
ancestors, the pattern of *differences* in proteins with the same
function, is essentially an inevitable consequence of random fixation
of selectively neutral sites (no need to invoke selection at all) and
the rate of such change is well within the *observable* rates at which
such events (selective or neutral fixation) would happen. [All he
would have to do is demonstrate that there actually is consistent
evidence that the earth is only 6000 years old to falsify this. And
to demonstrate why all the current evidence pointing to much longer
time frames is misleading.]

Neutral evolution or "random walk" doesn't really help, statistically,
to find potentially beneficial islands in the vastness of sequence
space any faster that any other search algorithm.

But combinatorial variation does. And finding what functional
variations nearby that can be reached have potential utility does,
since the beneficial island for, say, the aldosterone receptor protein
overlaps with the beneficial island for the cortisol receptor
protein. Such overlapping functionalities are quite common in the
*real* world of *real* enzymes, which almost always have secondary
functionalities and have effects on substrates other than the primary
one in current use.

Duplication and subfunctionalization or neofunctionalization are
common events. For example, this explains the current structure of
hemoglobin in mammals, with its IC structure of two alpha and two beta
globins (as well as the changes in beta globins during development).

Most features of *real* evolutionary change are primarily quantitative
or involve timing in nature. The sequences that regulate gene
expression are short and can be affected in a quantitative rather than
a qualitative way.

Similarly, changes that affect aggregation and interaction of proteins
are also short and can be changed in a *quantitative* way to produce
greater or lesser affinity.

It seems to me this is approaching the problem backwards. There is no
algorithm attempting to find anything. There is no goal. The mutations end
up where they end up. Whatever interesting behavior that happens along the
way is what happens.

Sean, like all creationists, greatly exaggerates the amount of
"novelty" that exists in nature at the molecular level and assumes
that one cannot reach a current structure by modification of a
previous one(s). He, in particular, assumes, although he denies it,
that the only way to produce a new function that he names is to start
at some random sequence *of the same size* some unknown distance away
and proceed in a single-step manner. In fact, his model of how
"evolution" works is absurd and has no relationship to any real
*evolutionary* model for the generation of new or modified function.
That is why I consider what he is doing numerology rather than
science.

For example, despite the fact that a lactase enzyme might be useful in
a particular gene pool in a particular environment, that function will
not exist with any arrangement of just 40 or 50 residues . . . or even
100 residues. The same thing is true of flagellar motility. This
type of function cannot be realized with the use of just a 400 or 500
or even 1000 codons of DNA - regardless of arrangement.

So what? Perhaps some other non-harmful function can be realized with
fewer
codons.

That's fine. If all that existed where functions that required no
more than a few hundred fairly specified residues, the ToE would be a
perfectly reasonable explanation.

The vast majority of proteins are 300 +/- 200 aa in length. And
ICness in multiprotein systems can arise by the initial effect of an
associating protein merely being 'helpful', with subsequent changes
making it 'necessary'. Or, like the eubacterial (and, independently,
the archaean flagella) being the consequence of a linkage of pre-
existing subsystems that do not need to change what they do,
converting the problem to that of producing one particular protein (a
chimeric one at that, and chimeric proteins are not produced by
starting at some random sequence of a random size).

The problem is that functional
systems exist that require very large minimum threshold requirements.
The question is, can the proposed evolutionary mechanism explain these
higher level systems? Sure, evolution doesn't have to produce higher
level systems, but can it? That's the question. Could the
evolutionary mechanism move beyond systems that have very low minimum
threshold requirements to come up with higher level systems?

Sean, of course, has no idea what he means by "higher level system"
when it comes to *function*.

The idea is that the function evolved from a different one. There need be no
minimum. Why is that so hard to understand?





*All* potentially beneficial systems that have higher minimum
requirements will be more widely separated in sequence space compared
to lower level functions - much much more widely separated (on
average).

Notice that Sean here is implying a model for how *he* thinks
evolution works. That it has no relationship to how people who
understand evolution and how new proteins in real cells arise doesn't
seem to bother him. He prefers his strawman, because it produces the
numerology he wants. He seems to be fascinated by large numbers and
always works to produce them, even to the point of producing
*probabilities* of 10^23. ;-)

That means, the evolution of any novel beneficial system at
higher level requires many more mutations, on average, from the
perspective of any given gene pool.

You have not demonstrated that there are *any* systems that have minimum
requirements for being either (a) beneficial, or (b) not harmful.

There are lots of beneficial systems, like flagellar motility, that
also have very high minimum structural threshold requirements coded
for by a minimum of well over 10,000 codons, or 30,000 bp, of DNA.

Originally, of course, this was 30,000 codons. Again, Sean does like
his numbers large, even if the large numbers are irrelevant.

Again, the argument that such systems didn't have to evolve doesn't
address the question of if they could have evolved via random mutation
and function-based selection.

What is so difficult about flagellar motility evolving from a similar system
that had a slightly simpler structure and performed a slightly simpler
function?

Or, as has been observed to happen, by the generation of a chimeric
linker that links the motor function and its proteins to the rotatable
pore and its proteins.

.

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