Re: Thermodynamic vs. Informational Entropy - for Dr. Marc Buhler




Marc wrote:

A germline requires germ cells i.e., gametes. Tell me again, how do
bacteria reproduce? How can those bacteria evolve without a germline?
Odd, isn't it, that by your definition of evolution only sexually
reproducing creatures are capable of evolution?

So, you are telling us that sex (defined as the exchange of genetic
material by individuals within a species) does not occur in bacteria?

I didn't say that. What I said was that bacteria that do reproduce in
a clonal fashion are evidently incapable of evolution via random
mutations and natural selection according to your definition. It seems
that according to you, evolution requires the ability to exchange
genetic material between individuals within a population.

Let's take a specific example, shall we? Consider Barry Hall's work
with E. coli and the evolution of the lactase function. This lactase
function evolved via a single point mutation over one generation of
bacteria which only used clonal reproduction without the need for
lateral genetic transfer to gain this function. Now, according to your
definition, this sort of evolution really wouldn't count as "real
evolution" because only clonal reproduction combined with random
mutation and function-based selection was needed here. No sexual
reproduction was involved at all. Therefore, according to Dr. Marc, no
evolution happened? Really now! ; )

You must have forgotten about how the bacterial chromosomes
were first mapped out. Strains of bacteria with known mutations
in specific genes were allowed to intermingle for various periods
of time, with the exchange of genetic material being scored in
terms of how long it took for a specific donor gene to reach the
point at which it was passed into the recipient. They did these in
the wife's Waring blender, IIRC, as they needed to be able to disrupt
the exchanges at a given moment and a blender worked quite well.

So now can you please agree that bacteria altering their germline
does in fact include "sex" and fits quite well with "my" definition
of evolution. How's your theory of "evolution plus design" doing?

Of course bacteria can undergo sexual reproduction, but they generally
reproduce in a clonal fashion. Beyond this, bacteria can evolve novel
functions without the need of sexual exchange of genetic material.
But, according to you, this type of evolution wouldn't count?

You've just painted yourself into a corner on this one and must be
simply trying to save face here. Not even those who are generally on
your side in this forum (just about everyone) agree with you on this
one. Do you know how often antibody evolution as has been used by many
in this forum as an example of evolution in observable time? Are you
going to take that away from them? You see, you aren't really hurting
my position at all with this strange notion of yours. You're damaging
your own position if anything.

I'm not quite sure how I've defined or used the term antibody in any
unusual way. Antibody specificity, with regard to a specific antigen
epitope, can certainly change over generations of immune system cells
via random mutations and function-based selection.

Sean, you need to re-read that chapter on the specific B-lymphocyte
mechanism of mutation of an antibody binding pocket (it's "somatic
hypermutation", as I've mentioned before). This "hypermutation"
process is *not* random mutation.

Somatic hypermutation is most certainly random within a limited range
of positions.

You also seem to overstate the
"function-based" aspect of this process. It's just the fine-tuning on
an immune response and while you seem to agree now that no
new function per se is gained, you still seem to think it shows some
(important?) point, which it doesn't.

Fine-tuning of a function is still a change of a function toward or
away from the most ideal form of that function. A fine tuned change is
still a change in beneficial function as far as degree is concerned -
it is change that most certainly has an effect on function,
selectability, and reproductive advantages.

I would also question (again?) if your "generations of immune system
cells" is really meaningful. Maybe I haven't taken you to task on this
point yet, but in your "normal immune system" these responses ebb
and flow, but do not go on and on for generations and generations.
For the most part an immune response continues to target the original
antigenic epitope and doesn't go shifting to other "functions", as
picking up new targets for an immune response would have some
profound risks. It may also be that there is a limit to generation
numbers in your "changes over generations" argument, and that
after a certain amount of possible change, that lineage is over.

It doesn't matter if the numbers of generations are limited. The fact
remains that these changes do indeed occur over a few very real
generations of immune cells - passed on from parent to daughter via
clonal reproduction. There is no fundamental difference here vs. the
way Hall's E. coli evolved the lactase function over a very few
clonally reproduced generations of bacteria.

While I agree with
you that this really doesn't count as the evolution of a new type of
function, it most certainly counts as a functional change over
generations via random mutations.

Again, while you finally concede to my point about evolution (in an
offhand way),

I've said this about the immune system function way before you came on
the scene here Dr. Buhler. I've always maintained, from the very
beginning, that no new type of function was evolved by the immune
system - only the refinement of a pre-established function. This,
however, is most certainly still a type of evolution.

you continue to mistake a changing function of an
immune response as some sort of good thing. As mentioned above,
it's not. It doesn't happen a lot but has the risk of autoimmunity when
it does. Somatic hypermutation cannot be used endlessly without
disrupting the very nature of "self".

You are both correct and incorrect here. Somatic hypermutation must be
limited in a tightly controlled way or autoimmunity would result and
the whole organism would undergo meltdown and rather sudden death.
However, somatic hypermutation can be and is beneficial if it is done
in a controlled way. Refining a response to a specific antigenic
epitope is very helpful. It is important for the development of
immunity - for example.

............ snp the rest.

It's ironic that your "crossing the gaps" argument works really, really
well with regard to the vertebrate adaptive immune system's use of
lymphocyte clones with unique antigen receptors. At the dawn of
the evolution of vertebrates, with adaptive immunity in the various
invertebrates able to provide some limited defenses against many
pathogens, the evolution of the adaptive system brought on from
the aftermath of the early vertebrate genomic duplications (along
with the establishment of the vertebrate body plan) gave rise to
this system of producing clonal antigenic receptors to effectively
all possible antigens, even those as yet unseen.

All possible antigens? - Are you agreeing with me now Dr. Buhler?

This happened
in stages, of course, and goes on even today with pathogens in
an endless attempt to shape-shift or otherwise avoid our immunity.

Nice story telling with absolutely now observable demonstrable evidence
to back yourself up beyond sequence comparisons. At lease some of the
authors who wrote the references you list are able to admit this. At
least they say this notion is a mere "assumption" based on sequence
comparisons. It has never been demonstrated beyond very low levels of
functional complexity.

Of course, you snipped that part of my discussion. So, I guess you are
going to continue to claim that I never define my terms? Remember now,
functional complexity is not the same thing as sequence complexity.
You need to understand the difference here.

The point here is that it is impossible for higher vertebrates to
evolve new specific binding pockets to a given pathogen de novo
and then to integrate those into the cellular or humoral immune
systems by recapitulating the steps required for specific function
by mutations over generations. A perfect example of just how right
your "crossing the gaps" idea is, albeit at a somewhat different level
of complexity than you allow for. Vertebrate evolution had to cross
this gap for itself somehow, and the whole system of education in
the thymus, peripheral tolerance, MHC-defined immune repertoires
of clonal binding pockets and all the other features of vertebrate
immunity has evolved in defiance of your big "gap".

So your story goes. Again, this story of yours is based on an
assumption that this happened without really going into what mechanism
could have really crossed such an enormous gap - a gap that you
yourself have just described. You simply assume that this gap was
indeed crossed by some series of random mutations and function-based
selection based on sequence comparisons, but you never go into the
details of how this could possible have happened without any outside
informational input.

Now, that's enough for "my" definition of immune evolution.

How's "your" definition (for today) of evolution going, Sean?

Is the above a valid example of "crossing the gap" or not?

It would be if you had anything other than sequence comparisons to go
on. You don't. You also do not evidently wish to get into the actual
mechanism that could have crossed this gap. The mere statement that
"gene duplications" where involved just doesn't cut it. Such bald
statements have no explanatory value here Dr. Buhler. The question is
how? How do gene duplications combined with any other type of mutation
you want cross these gaps? What are the odds that the right gene
duplication will come along and copy just the right genetic sequence
and modify it just right or insert it just right somewhere else so that
a truly novel high-level system of function is realized? That's the
real question. You don't seem to want to actually get into answering
that question. Why not?

(signed) marc

Sean Pitman
www.DetectingDesign.com

.



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