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


Seanpit wrote:
Marc wrote:
Seanpit wrote:
Marc wrote:

Warning to those with weak hearts. I am going to mostly agree with
Sean in this post. Not, of course, that that helps his larger argument
(as I point out). It is possible that I merely got in on the tail end
of this very funny, very Ferric discussion.

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.

I get the feeling that your starting yet another new thread directed
to me is to break away from the comments in the previous thread
so you can better try to put words I did not say Into my mouth.

You were the one who said that bacteria didn't include "sex" in their
evolution,


I never said that bacteria did have the ability of lateral genetic
transfer.

It is called "horizontal" transfer. What bacteria do not have is a
regularized sexual mechanism similar to meiosis (itself a modification
of mitosis). Instead, genetic information exchange is a consequence of
episome transfer (episomes are sort-of benign -- usually -- viruses
that require direct cell-to-cell contact to transfer), direct DNA
transformation (in nature, only some bacteria do this), or transfer by
defective viruses. Such horizontal transfer can be within a "species"
or within a larger grouping of bacteria. But bacteria most certainly
can evolve vertically, that is, by changes in the population by
mutation (including endoduplication and chimeric rearrangement of
genes) of the existing genome and selection for variants thereof.

I myself have pointed out many times in this forum and on my
website that bacteria most certainly can achieve lateral genetic
transfer.

Your problem is that bacteria do not need to use this sort of "sex" in
order to evolve novel functions.

True. They don't *need* horizontal transfer to evolve novel functions.
Novel functions in bacteria *can* arise by vertical descent with
modification. However, evolution involving horizontal transfer is much
more common (a larger fraction of evolutionary change is due to
horizontal transfer) in procaryotes than eucaryotes. The most
spectacular (and medically important) example is the ability of
multiple antibiotic resistance to spread to new species via episomal
transfer.

Bacteria primarily reproduce via
clonal reproduction. Using only clonal reproduction bacteria can
indeed evolve novel functions.

Like eucaryotes where, except for the spectacular changes wrought by
integrating bacterial genomes from mitochondria and chloroplasts, most
evolution is due to vertical events. This is easier in eucaryotes
because of the presence of introns and because they have larger
genomes, thus having a larger pool of functionally active moieties from
which novelty can be generated. Also, because they don't as often
specialize for small genomes, significant numbers of duplicate genes
are a common feature of eucaryotes.

There is no fundamental difference here
between how bacteria can reproduce and evolve and how immune cells can
also reproduce and evolve.

Except for the fact that immune cells can only evolve so long as their
environment (the soma of a eucaryotic multicellular) continues to
exist. Any novelties (and there are many) that 'evolve' via random
mutation and selection during the lifetime of the host dies with the
host, since the germ line does not have the genetic variants present
and accrued in terminal immune cells.

It doesn't matter if the host cannot pass
this information on to its offspring.

Except for the fact that this puts a severe time limitation on the
ability of the immune system to generate all the variants it does to
respond to the wildly disparate selective environments it gets exposed
too.

The population of immune cells
CAN pass on this information to its offspring. Your reference to these
offspring as "daughter cells" is a strange attempt to ignore that these
daughter cells are indeed offspring in every sense of the word.

Daughter cells are indeed offspring. Just as daughters are.

They
are clonally reproduced offspring just as any bacterium is almost
always a clonally reproduced copy of its parent ancestry - save for
random mutations.

But, WOW! Think about it. Purely by the process of random localized
hypermutation, not even everywhere in the immune molecule, but mostly
within a stretch of about 30 aa's, followed by selection for variants
that bind a ligand -- even ligands that have never existed in nature,
about as novel as you can get -- one can generate proteins that bind
ligands tightly enough to act as enzymes. [In fact, most of the time,
the binding is too tight to be useful for enzymatic activity. But some
immune molecules do indeed act as enzymes, and it is possible to
generate selection that can do this, by binding to a chemical
transition structure.] This occurs, not over generations, but within a
single generation. All by the very mechanism that you claim cannot do
such feats in trillions of trillions of years.

nit-picking on the germline comment and my citing of the
Wikipedia definition in the other thread.

You, being trained as a Doctor, should know that a "germline" usually
refers to reproduction with the use of gametes. Germlines simply
aren't necessary for an organism to undergo "evolution". Despite the
fact that sex allows a more rapid dissemination of new beneficial
genetic material, sexual reproduction simply isn't necessary for
evolution to occur. Also, sex doesn't help evolutionary mechanisms
find novel functional sequences any more quickly. It only helps in the
distribution once the novel functional sequence actually enters the
gene pool. I'm only interested in when the function first enters the
gene pool - not so much how long it takes to distribute this sequence
throughout the gene pool.

Another of your tricks, Sean,
is deleting material in the earlier post and not indicating such.
Let's have a look at that.

Oh come on now. I can't respond to everything. You yourself snip a
great deal of my posts all the time - this thread is no exception.

I think his complaint is that you do not mark that you have snipped
material. He has good reason to be upset at such a practice.

You
still haven't responded to the part about the difference between
thermodynamic and informational entropy or the difference between
random sequence complexity and functional sequence complexity.

Here is a passage from my earlier post in this thread:

"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?"

Sean, the word "include" isn't there to mean "depends on", is it?

That's my whole point. If evolution doesn't depend on sex; if evolution
can happen with the use of clonal reproduction alone, then your notion
that immune cell populations cannot evolve novel functions is
erroneous.

Exactly how does this help your larger argument, Sean? *Changes* in a
mere handful of aa's in an otherwise unaltered larger protein (which
would have a much larger number of 'fairly specified residues') can
produce variants that can bind pretty much any biologically meaningful
molecule and even molecules that have just been invented by humans.
That doesn't sound like a case where the number of 'fairly specified
residues' can tell us anything useful about how many *mutational
changes* were required to generate a specific novel selectable
*function* to me. Can you tell me how the two numbers (number of
'fairly specified residues" and number of mutational changes) are
related to each other and to the evolution of functional endpoint
(clearly not a teleological or pre-planned or designed one) in
immunoglobins?

The point is that immune cell populations do in fact
reproduce and pass on genetic information from parent to daughter via
clonal reproduction. This means that this population can indeed evolve
novel functions just like any other clonally reproducing population,
like bacteria, which even you must admit can evolve. If bacterial
populations can evolve via clonal reproduction alone, then how on Earth
can you argue that immune system cell populations cannot really
"evolve"?

Evolution does greatly benefit from the exchange of genetic material
but that isn't saying the mutations which occur and are passed to
the daughter cells isn't a part of prokaryote evolution - your whole
post here is based on your lack of comprehension of what the word
"include" was about. Nice move to delete that bit in this reply.

There you go. If mutations which occur and are passed to the daughter
cells IS part of prokaryote evolution, then how can you argue that
mutations which occur and are passed on to daughter immune system cells
does not qualify as real evolution within that population? Just
because the host that contains this population doesn't pass this
information on to its offspring doesn't mean that the subpopulation
isn't really evolving. It is.

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! ; )

Again, it's a shame you twisted things around such that you feel this
passage is necessary. It isn't. (But you knew that, didn't you?)

Yes, I did know that. You have to admit evolution in the case of
bacteria, but you fail to see the parallel with immune system cell
populations. There is simply no difference between one and the other.
That's the point.

Perhaps I have contributed to the confusion here by assuming that
you would understand my intention in a comment about "germline"
that referred to prokaryotes. I'm not sure what term to use in place
of germline in that context, but for whatever degree I am in error in
this, your comments are much more in error.

Your error is that you fail to see that populations of immune system
cells are not fundamentally different, with regard to evolutionary
potential, than bacteria that evolve novel functions without the aid of
sexual reproduction.

And I agree. But what do these facts have to say about your idea that
evolving new function by random mutation (wrt need, not rate) and
selection cannot produce 'novelty' of function in less than a trillion
trillion years?

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?

Not according to me - according your misunderstanding of my comments!
You do get quite stupid at times, Sean.

At times? ; ) I didn't misunderstand your comments Marc. I
understood you quite well. I'm just showing that your notions are
inconsistent with each other. On the one hand you believe in the
ability of prokaryotes to evolve without the need for sexual
reproduction while at the same time holding the notion that a
population of immune cells cannot really evolve novel functions over
the same number of generations of immune cells.

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.

I think most of them agree about how you twist things, about the
stupidity of your position in disregarding sequence-based data etc.

Yeah, but they don't agree with you on this particular point. Most in
this forum believe that immune system refinement over generations of
immune cells does in fact count as real evolution. They use this all
the time as a glowing example of observable evolution.

Well, it is certainly a glowing tribute to the capacity and speed of a
mechanism involving both random (wrt need) mutation and natural
selection to generate genetic variants with a novel function wrt which
epitope an immunoglobin binds. All accomplished without the variants
being noticeably designed by any agent nor present in the initial
starting population (the original germ cell's genome before the
alterations that occur in the white cell lineage).

For me, I
really don't care since this has nothing to do with my main point here.
If you want to argue that immune system changes over time doesn't
count as real evolution, that's fine with me. It actually goes in my
favor. Thanks! - though I really don't agree with your efforts in my
favor in this case.

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.

No, I don't know how often that argument has been used but since
it has no basis in fact, I really don't care how often - or by whom -
it has been used. You seem to have switched back and forth a bit
as to who was using it, anyway - you or some others - but, now
that you have admitted it isn't a facet of ongoing evolution, it's time
to drop that issue.

I never said that immune system evolution was a facet of ongoing
evolution. Why build these strawmen? What I said was that it was a
facet of evolution of a specific population over a limited span of
time. Just because a population may not survive very long doesn't mean
that it didn't evolve in the short span of time it existed.

And what an enormous range of genetic and functional novelties is
produced in that short span of time!

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.

In the evolutionary sense of the word "random", which refers to
mutation being produced according to need, hypermutation is random
mutation. Hypermutation is a change in the mutation rate of a local
region. It is not generating specific mutations that are needed in
response to an environmental stimulus. It is generating all sorts of
variants and selecting, among them, the cells producing the
immunoglobin that binds the environmental stimulus epitope. Mutation
rates, even outside this particular gene segment, vary widely from
local site to local site. For example, the dominant mutation for
achondroplastic dwarfism, a single specific point mutation, occurs at a
very high frequency relative to most identical point mutational
changes.

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

Thank you. A concession. Mutation in B-cells is limited. This is good.
(See the abstract right at the end of this post, too.)

I never said otherwise. Again, you attempt to build a strawman here.
You are the one who said here that, "This 'hypermutation' process is
not random". Well, of course, that isn't quite true. Hypermutation in
this case most certainly is random. Though limited, it is random. So,
your statement here isn't quite accurate.

I certainly agree with Sean here. Hypermutation refers to the *rate*
of mutation being high. The only examples of specific mutations
occurring this way involve domesticated mutational events like the
mating type switch in yeast or the inversion that changes surface
antigen of mu phage or the changes in trypanosome surface antigens or
the induced induction of transposon activity in corn. Most of these
have a degree of randomness wrt when they occur (in a stochastic
sense).

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.

I have no idea what Sean means by "the most ideal form of that
function". Wrt epitope binding, the epitope bound can be almost
anything large (and a number of small things, when attached to
something bigger) that interacts with biological systems. What is the
"most ideal form", given that it can bind almost anything? Perhaps
Sean thinks that the initial sequence in the germline is the "most
ideal form"?

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.

What is it with you, Sean?

We get to a point where you admit that modification of antibodies
isn't a part of germline change or contributing to evolution and then
you try to slip "reproductive advantage" back into the discussion.

What is it with you and this "admit" stuff? I've never said otherwise
so how can I be "admitting" anything here? I've never said that
antibody changes were part of the "germline" of the host individual.
The fact is, Dr. Buhler, the immune system cells, as part of the
subsystem population of the host, do indeed pass on genetic information
to their own offspring cells via clonal reproduction. Certain genetic
changes do indeed give certain offspring cells a reproductive
advantage, not to the host, but to these individual cells relative to
their immune cell peers.

This is all quite obvious to the candid mind. How you can get so
confused over such a simple concept, especially with your professional
training, is beyond me.

You are also trying to bring the "function" argument back from the
dead here, too. Why? You admit something is wrong, then turn
around and use the argument again as if it is now somehow right.

Again, I never admitted that anything I said was wrong here.

You do indeed seem to have the "doctor is god" act down pat.

I've
always said the very same thing. The change function we are talking
about here obviously gives a reproductive advantage to the immune
system cell in the immune system population of cells.

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.

The difference has to do with evolution, Sean.

It's not too hard to follow, but you have to stop mixing around the
various ways the word "evolution" can be used and stick with the
biological traits inherited over time concept. Please.

Your bacterial example (which I won't bother to read more about or
to nit-pick how you describe it) is one where there is evolution going
on in that a change is passed down to future generations of organisms.

Exactly! In the same way changes in immune system cells are also
passed on the future generations of cells in that population of immune
cells. Just because a population of bacteria happens to get whipped
out after, say, 10 generations doesn't mean it didn't really "evolve".
If Hall had whipped out all of his bacteria, sterilizing everything,
after he was done with his experiments, would this mean that these
bacteria hadn't really "evolved"? Of course not. In the same way,
just because the changes in the immune cell population ends up being
lost when the host dies, does this mean that these changes really
aren't "real" evolution in action? Of course not . . .

The humor in Sean's response is just filled with Fe.

Perhaps you could say a change in the germline has been made here
and be understood, despite there being no "germ cells" in prokaryotes,
but since prokaryotes do have exchanges of genetic material ("sex")
as well as other means of altering traits in evolution, they could be
considered to be their own germ cells and thus allow for the comment
(that a germline change has been made) to stand. [I may need some
help from Dr. John here on how the term "germline" fits or not.] Still,
to compare evolution in prokaryotes with that of vertebrates and their
ability to make antibodies, understanding that a trait is only able to
be inherited when it is a part of the germline is important.

Not when you aren't looking at the organism as a whole. We are only
considering a population of cells within an organism that reproduces
and evolves in very much the same way as prokaryotic single celled
organisms usually reproduce and evolve.

As I have explained several times recently in the other threads, there
are no "antibody genes" in the vertebrate genomes. Do you agree?

There are gene segments for different parts of the overall antibody
chains (and TcR chains), with Constant, Variable, Diversity and also
Joining segments of different sizes, plus random nucleotide insertion
that takes place amongst the V-D-J-C recombination steps to build
the unique antigen receptors in a clonal fashion. (One cell has just
one receptor, and that is the one the daughter cells will also have.)

I cover this in some detail on my website:

http://www.detectingdesign.com/immunesystem.html

This happens in somatic cells, Sean. Material that was once located
between the segments is deleted from the genome in these cells,
but that deletion does not reflect any germline alteration, does it?

Why are you so hung up with the germline thing? I never said that the
germline was involved here. It isn't. We are only talking about
evolution within the population of immune system cells here. It
doesn't matter that this isn't passed on via the germline. It is still
the evolution of a novel refinement of a function that wasn't there
before via random mutations (limited though they may be) and
function-based selection.

Offspring will not have any changes to their inherited genome from
any reaction of a B-cell or T-cell with antigen that occurred in their
parent, right? Could you please clearly state that you agree with this.

The host offspring will not have these changes, however the offspring
of the immune cells will have these inherited changes. Don't you get
it? We are only talking about a special population there - the
population of immune system cells. We are not talking about the
eukaryotic host organism here.

If there are no germline mutations or alterations, then please now
explain how "evolution" has taken place between the parent and the
offspring with respect to antibody binding sites or antigen receptors
from T-cells. That is the form of "evolution" to consider here, Sean.

No. The form of evolution we are considering here is the evolution that
occurs between parent and offspring immune cells. You say that immune
cells do not have "offspring" since they are called "daughter cells".
This is just amazing! Come on now Dr. Buhler! Don't tell me that
calling something a daughter cell really means that it isn't an
"offspring"! Sheesh! What do you think the term "daughter" means?

If it is *not* passed on as an inherited change, please avoid the use
of the term "evolution" in this discussion. Swapping definitions is a
ploy of yours, Sean, and you are not to do that again here.

The changes are passed on as inherited changes from parent to daughter
immune cells - Dr. Buhler. This has nothing to do with swapping
definitions. Your attempts to obfuscate by asserting that daughter
cells aren't "offspring" are simply ludicrous for someone of your
educational background.

< snip >

(signed) marc

Sean Pitman
www.DetectingDesign.com

.

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