Re: Cope's rule and bacterial evolution

Until and unless some mechanism is found whereby a phenomenon occurs
(be it increasing in size or complexity, or be it shedding of genes or
excess complexity or be it any other "quasi-strategic fortuity
availance" (QSFA) then any implication that the QSFA is being done
because it is advantageous is at least as unscientific as the ID
positing of "G-d did it" (GDI).

Note: This kind of debate really belongs in talk.origins.
Maybe the moderator can cross-post there to start miagration to there?

Anyway, do you agree that sometimes the mechanism that replicates DNA
occasionally slips backwards (causing a short repeat) or forwards
(causing a point or short-sequence deletion) mutation? So there's your
mechanism for introducing longer or shorter sequences into the genomes
of the population of various cells in a clade.

Do you furthermore agree that any fatal mutations are eliminated within
a single generation, so only non-fatal mutations survive over multiple
generations? Likewise disadvantageous though not-immediately-fatal
mutations will die out in a few generations? Do you furthermore agree
that if by chance one of these indel mutations is an advantage, either
in trimming down a too-long genome, or in enhancing a genome by adding
something new, the clade with the mutation has a good chance of
producing more members than the clade without the mutation,
exponentially more over long time spans, and driving the non-mutated
clade to extinction as soon as the mutated clade has grown large enough
to exhaust all resources of the shared niche? So there's your mechanism
for evolving toward better fitness via either trimming a too-large
genome down to more efficient size, or enlarging the genome if that
results in some improvement.

How exactly are these mechanisms no better than GDI?

Re GDI vs. Darwinian mutation+selection:
the former conceptually putting the reins in the hands of a deity,
and the latter putting the reins in the hands of organisms themselves.

I don't know what you mean by reins here. With mutation+selection, its
the environment, the circumstances affecting the individual, that
determines which directions of change are favorable and which
directions are unfavorable. Mutation simply tries lots of different
directions at random, and selection is what we call the differential
survival due to the environment. If we use the metaphor of "reins", at
best it's the environment that holds the reins, but it's not reins in
the sense of deliberately directing evolution, it's more analagous to a
minefield, whereby some directions of wandering immediately hit a mine
and are blown up, while other directions get so far from any high
density of mines that they allow much more freedom of wandering with
few deaths thereby allowing those populations to grow without the
severe attenuation of growth caused by frequent hitting of mines. There
aren't any reins pulling individuals away from mines. It's just that
any individual who happens to wander far from mines thereby achieves a
nice safe place to raise children, and grandchildren, etc., so after
much time the families living in the densest parts of the minefields
become rare while the families living away from mines become common.

Bio-evo theorists are applying a double standard if they condemn the
ID view (putting the deity in the gaps) yet turn right around and
insinuate that bacteria or viruses dispose of gene baggage they can do
without

All we say is that they randomly dispose of one bit or another of their
genome, and if they dispose of an essential part they die promptly,
while if they dispose of something they don't happen to need they have
more offspring than any brothers without that mutation. What part of
that do you dispute??

or that complex phenotypes mold themselves to avail themselves of
niches, or increase their capacity to tolerate some challenge.

Nobody except misunderstanderers-of-Lamarck would make any such claim.
You are using a strawman here.

And I would wish to see my favorite science team -- or, okay, one of
them -- avoid the APPEARANCE of assuming a double standard.

In this case, appearance is entirely in the perverted mind of the beholder.

One poster recently ... sought to persuade me that the fact that H.
sapiens cannot make their own ascorbic acid is because... vitamin C is
abundant in their diet under most circumstances

Slight correction to your parahprase of what somebody else said:
For several million years in the *past*, our ancestors all lived in
abundant tropical rain forests in Africa, eating fruit which contained
lots of vitamin C. It is only starting about four million years ago,
during a period of drought, that our ancestors moved out of the
fruit+rain-forests, and learned of our need to take special measures
to get enough vitamin C, and it had been such a long time since we had
a working gene to make it that a simple mutation or two couldn't get it
back to working again.

The fact that H. sapiens could get along without making their own
ascorbic acid does NOT explain how, nor why -- as the case may be --
any of our anthropoid ancestors had it and lost it

Have you ever heard of "point mutation"?? You don't need a deletion event.
A simple point-change in a DNA base is sufficient to disable a working
enzyme in a biochemical pathway. That was an advantage, because too
much vitamin-C is slightly toxic, and we already had more than enough
in our fruit diet and actually needed to spend energy excreting it. The
mutation saved us both the energy needed to make it and some of the
energy needed to excrete it.

By the same token, merely demonstrating that it is mathematically
POSSIBLE for a single mutation, in a single individual, to become
spread throughout an entire population does not explain that it
actually DID happen.

That's correct. It's a matter of chance whether any particular kind of
mutation will actually happen during a given span of time (although
it's inevitable that *every* kind of mutation will eventually happen if
a clade survives forever, and nearly inevitable during a span of five
billion years from the first animals to the end of the Sun's lifetime).

Our ancestors had only about 50 million years in the rain forests, so
some of them lost their vitamin-C synthesis ability and some retained
it, as a matter of chance. Our particular clade lost it. More info:
<http://www.grisda.org/origins/12096.htm>
The standard comprehensive reference on comparative physiology
(Prosser 1973) states that ascorbic acid is synthesized in adequate
amounts by most vertebrates, though required in the diet of man,
monkeys, and guinea pig. ...
In the last half of the decade three comprehensive papers on
mammals appeared, all by Birney et al. (1976, 1980) and Jenness et al.
(1980). They could detect the critical synthesizing enzyme for
ascorbic acid in only 1 of the 34 species (6 families) of bats
studied, and there only a trace was present. ...

The article goes on to discuss how vitamin-C is made in the liver or
kidney (or neither) in different clades of animals. Then it concludes:
Is this pattern produced by degenerative loss of synthetic
capability? The evidence indicates that it is. ...

To say it is energy conservation by default, in saving the energy
that would be required to make ascorbic acid when none was needed, is
ONCE AGAIN to pose that a population would proactively do what is
necessary to make such a miniscule energy saving.

You're attacking a strawman. Nobody claims any life proactively changes
its genome. We all (except Creationists and IDiots) say life randomly
chances into various changes, and there's a bias toward keeping the
good changes and discarding the bad changes.

I hope humans will not, as a result, lose the capacity to convert
starches to sugars, due to the fact that so much sugar is available in
most humans' daily diet. (I will stipulate that if it were to happen,
it might take a million years or more, so I'm not just summonsing a
short-range view. Nor am I meaning to imply that we may not be
gravitating in that direction in increments to small to measure. Maybe
we are.)

In this case you're almost exactly correct. It would take a very very
long time, both for significant chance of such a mutation happening and
lasting enough generations to avoid prompt extinction, and then for
such multi-copy new allelle to spread through the population.

... just because an organism makes a change, and that change provides
some benefit, that does NOT prove the organism made the change as a
result of the fact it foresaw that it would be "nice."

That's the misunderstood-Lamarck strawman again.

when biologist (one of my favorite teams) make a comment along the
lines of saying, for example, that "viruses are disposing of their
excess baggage," they qualify that by making the disclosure, "... but
we do not know yet exactly why or how..." (Or if we do know exactly
why and how, as supported by an abundance of empirical evidence, then
let us say that, and produce our evidence.)

There are multiple mechanisms already known for deleting small sections
of a genome. I mentionned forward-slippage of the DNA copying mechanism
earlier. Another is accidental cutting of a DNA chain in two places and
losing the middle place and accidently splicing the two end pieces back
as if whole again. The best we can demonstrate when looking at before
and after sequences of a mutated virus is that a particulr sequence
which was present is now gone. There's no way we can run time back and
look at the actual deletion event in an electron microscope to
determine for sure which of the two or more known mechanisms actually
was responsible for that particular event. You're asking for miracles!

Otherwise, we make the same mistake (or appearance thereof) as the
ID'ers, of substituting our own eclectic "choice of cause" for
theirs, to fill the potholes in our knowledge.

IMO that's a completely unfair judgement on biologists. The biologist
demonstrates, in the lab, several ways that deletions actually do
happen. The biologists go to a lot of trouble and expense to sequence
the virus at various times, and they discover a difference, of the
deletion type, between two successive sequences they have measured. The
biologist then says a deletion seems to have happened, probably by one
of the known and demonstrated mechanisms, possibly by a new mechanism
not yet discovered. The IDiot never demonstrates G_d doing any
deletions, yet claims GDI for sure, dismissing all the evidence the
biologist has already shown as to various known biochemical mechanisms
that could have been responsible.
How can you possibly equate biologist = IDiot?
..

.

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