Re: Darwin, NeoDarwinian Taboos, and the Explanation of Evolution




According to the theory:
1. Changes in conditions of living have no direct influence on
evolution, i.e. they cannot predictably change genes and the
information genetic.

That is correct in most cases. The mapping from DNA through RNA and
amino acids and proteins and embryological development is so
complex and mostly one-way (except DNA->RNA where reverse
transcriptase is known to exist), that it's inconceivable that
direct influence of phenotype would be able to directly change the
DNA in an appropriate way. Only modern technology with
understanding of how genes affect development and hence phenotype
could possibly directly engineer a mutation to effect a desired
change in phenotype. The possible exceptions would be direct
chemical acceptors based on shape of protein or RNA-enzyme. It's
known that some combinations of alums in solution will crystalize
into two different chemical mixes depending on the physical shape
of the a seed crystal, thus two different species of alum crystal
can crystalize from the same solution. It's plausable that some
bacteria might have a mechanism for "crystallizing" either amino
acid sequences or RNA sequences around a foreign toxin such as a
virus sequence, in a way that best fits that foreign toxin, thus
makes the best receptor for it. It's possible that some bacteria
might have capitalized on this idea by chancing upon a reverse
transcriptase from amino-acid sequences back to canonical DNA
triples. Then putting the two mechanisms together, a bacteria might
self-mutate directly to better recognize a newly-introduced toxin:
- Optimally "crystalize" amino acids or RNA bases around the toxin.
- Reverse transcript it back to DNA.
- Transport that DNA into the genome, in a location next to some
detoxifying agent.
- Now, and in later generations, this sequence of acceptor plus
> detoxifier will code for manufacturing a chemical that will
> attach to that particular-shape toxin then enhance its chemical
>disassembly or porting through the cell wall to the outside or
> through a vacuole wall to a generic chemical-decomposition
> mechanism. It seems to me the most likely mechanism, due to
>maximal re-use of old parts and minimal new custom parts needed,
>is to have two acceptors attached together, an "inside" acceptor
>that wraps around the shape of the toxin, and an "outside"
> acceptor that attracts a generic cleavage enzyme or a generic
> transportation carrier.

Sorry, but I was unable to understand whether you agree or disagree
with the above neoDarwinian principle.

2. Use and disuse of organs has no influence on evolution because
changes they produce (enlargement and vestigialization of organs,
respectively) are not inherited

Ample evidence shows that's most likely 100% correct.

I would appreciate you providing a little of the ample evidence that
=93Use and disuse of organs has no influence on evolution=94.

3. The evolution is irreversible (Dollo's law) due to the
random character of changes in genes.

That's almost true. Reverse of effective phenotype *is* possible,
and happens frequently. We call it "convergent evolution". For
example, fish evolved to reptiles, losing fins. Hippos evolved to
whales, inventing a different kind of fin all over again. By
chance, the original fins were vertical, generated by spine with
spikes protuding along the line of symmetry i.e. up+down, where
whale fins are horizontal, generated by two legs side by side, so
it's trivial to tell them apart. Likewise octipus and vertebrate
eyes evolved relatively inside-out where retina attaches, making
them externally similar (all you see is pupil and iris) but
internally quite distinct upon dissection.

First, what should one understand by =93almost true=94? Do you mean that
there are exceptions to Dollo=92s law=94. If so then that=92s not a law.
Second, evolutionary convergences are not synonymous to evolutionary
reversals, and
Third, your examples are not evolutionary reversals.

But over a very short term, when there hasn't been time for
vestigal genes to mutate too far, when the mutated gene is still
*slightly* functional, so that selection for function can
immediately act on that gene rather than on other possible
replacements, selection can revive the quantity of the
least-mutation best-still-functionning allelles of the
no-longer-vestigal gene in the population, and mutation might
possibly restore the original protein shape if not the exact
amino-acid sequence and surely not the exact same DNA sequence.
Since neutral drift can convert different amino-acid sequences that
have the same protein shape hence the same catalytic function, we
can regard all these same-shape allelles as "the same" gene, so
this is not convergent evolution, it's true reversion of an
ancestral genotype-cluster by restored selection. But this can
happen **only** after just a short time of drift.

I am sorry but I find it hard to follow your idea and understand terms
like =93vestigial genes=94, =93 the least-mutation best-still-functionning
alleles=94, =93no-longer-vestigal gene=94, etc. I cannot also understand ho=
w
gene drift can lead to evolutionary reversals. However, if I got it
right, you mean that evolutionary reversals can occur for evolutionary
short periods of time, an idea that has circulated in the last two
decades.
There is adequate observational evidence that evolution is reversible.
That evidence compelled even a neoDarwinist of high stature as
Bernard Rensch to downgrade Dollo=92s law into a =93rule=94. I will
illustrate the reversibility of evolution with only a few examples.
Warmbloodedness evolved and was lost in the class of fish to reappear
later in evolution of birds and mammals, implying that warmbloodedness
reappeared after evolutionarily long periods of time. Chondroichthyes,
cartilaginous fish, lost bones that were present in their ancestors,
then bones reappeared in Osteoichthyes and again were lost in
Chondrostean fishes to reappear in Teleostei.
Due to the complexity, interactions with other structures, and the
number of genes involved in the development of insect wings, it has
been considered that the reversion of wings in insects that lost wings
is impossible. However, some phasmid insects re-evolved wings after
having lost them.
Paleontological research provides rich evidence of evolutionary
reversals in gastropods.
Paleontological evidence exists on a case of reversion of limbs in
snakes.
Many bird species have re-evolved some muscles that were lost in their
ancestors. Reversion of lost digits is observed in guinea pigs.
Evolutionary reversals are described not only for morphological traits
but also for life history traits and even reversals of ancestral
genetic systems have been described.
It was believed that loss of structures was related to the loss or
occurrence of function-preventing mutations in genes. There is both
experimental and observational evidence that reversion of ancestral
structures is not related with changes in the function or the
structure of relevant genes. So, e.g., it has been possible to
experimentally induce the development of teeth in birds that have lost
these structures ~80 million years ago and observational evidence on
atavisms, reappearance of lost ancestral structures in individuals of
various animal species, including Homo sapiens, shows that all the
genes (and =93regulatory sequences=94 for that matter) necessary for their
development are functional despite the long time since the structures
were lost.
For further evidence on evolutionary reversal and the epigenetic
mechanism of evolutionary reversions see http://www.epigeneticscomesofage.c=
om

Despite the Darwinian label all the above neoDarwinian tenets
contradict and are irreconciliable with Darwin=92s own views as
he presented them in =93The Origin=94.

Darwin's book was a *first*draft* of the theory, and we can expect
lots of mistakes in emphasis and a few real bloopers. The "bible"
is the concensus result of the latest research as reported in
Nature and Science and Cell etc., not a first draft written 150
years ago. Darwin lived in a time of Lamarck, circa 50 years before
Mendel when genes were shown to be discrete and in linear chains,
circa 100 years before Watson and Crick discovered that those
linear chains were DNA polymers that code in triples for amino
acids, circa 150 years before Venter et al. who read out appx. a
hundred complete genomes including human. (Curious concidence: The
number of discovered planets around other stars, and the number of
complete genomes read out, are growing at similar rates. Which one
will greatly surpass the other?) It's understandable that he got
some of the mechanisms of mutation grossly wrong, even while he got
the mechanism of selection and evolution essentially correct in its
large form.

What you call Darwin=92s mistakes cannot be related to the fact that he
did not know about the discoveries of Watson and Crick and Venter et
al. (which are of little relevance to the Darwinian variability). He
was criticized in his lifetime by the co-author of the theory of
natural selection, Alfred R. Wallace which, like neoDarwinians half a
century later, rejected the Darwinian idea that =93natural selection is
not the exclusive means of modification=94. In this sense, stripping of
Darwinian doctrine of three of its basic principles reduced rather
than complemented his doctrine. In this sense the neoDarwinian system
is obviously closer to Wallace=92s than Darwin=92s concept of evolution.

In relation to the first NeoDarwinian tenet, Charles Darwin
believed that changes in the environment induce inherited changes
in living beings and these changes are not always random but may be
directed:

He was wrong about that.

I doubt that you can substantiate your statement that Darwin was
wrong.

He believed and presented examples that use and disuse of organs
can lead to inherited enlargement or vestigialization and loss of
structures, even not necessarily with the aid of natural selection:

He was wrong about that too.

Evidence or theoretical arguments are necessary to support your
statement.

When a character which has been lost in a breed, reappears after
a great number of generations, the most probable hypothesis is not
that the offspring suddenly takes after an ancestor some hundred
generations distant, but that in each successive generation there
has been a tendency to reproduce the character in question, which
at least, under unklnown favourable conditions gains an
ascendancy.

This seems to be a matter of low-frequency but not-yet-extinct
allelles being selected-for again ahd thus escaping extinction and
growing to large and hence noticeable fraction of total again.
Also, in some case, weakened genes being selected once again,
resulting in *selection* (not mutation) drawing the *phenotype*
once again toward optimal functionality, either by convergent
evolution, or by re-tuning the protein shape while ignoring change
in amino acids which don't affect shape enough to matter.

I cannot understand whether you accept or reject the Darwinian concept
of reversibility of evolution.

Has the genecentric idea, i.e. the idea that the evolution of
organic world is ultimately determined by evolution of genes,
found any experimental or theoretical support?

It depends on whether regulatory sequences count as "genes" just as
well as polypeptide coders and RNA-enzyme coders. If all count, then yes.

My modest question is: Can you bring a single example of a change in a
=93regulatory sequence=94 that has been causally related to (to have
preceded in time) evolution of a morphological or behavioral
character?

Without rushing to conclusions, a review of all the experimental
and theoretical work conducted during a century has failed to prove
the idea. We still have not a single experimental proof that the
evolution of a trait has been induced by the evolution of one or
more genes.

Please don't use the word "proof" regarding scientific theories.
It's simply not appropriate.
You need to ask whether there's sufficient evidence to provide
strong support for the theory and against any alternatives that
have been proposed. Alternatives might fail because they make
incorrect predictions (Lamarck's theory), or because they are too
ambiguous wishy-washy as to what they could possibly predict
(goddiddit because itpleasedgodtodoit or because itwasgodsplan).

If you can=92t prove (demonstrate and reproduce) what you are saying,
that means that you don=92t have facts. You are asking too much if you
expect that people will believe anyone=92s statements that cannot be
proven. I would patiently listen to any hypotheses and statements but
I know that in absence of facts our discussion would lead us to
nowhere.

To the contrary, adequate experimental evidence shows that
various characters have evolved despite the fact that genes
involved in the development of these characters remained
functionally unchanged.

I suspect you are dismissing regulatory sequences as "genes", hence
this faulty conclusion. It's only a brief time (maybe 3 or 4
decades) after Watson+Crick and before Venter et al when we knew a
lot about DNA -> RNA -> polypeptides -> proteins=3Denzymes and very
little about regulatory sequences that we tended to define "gene"
as only the DNA...proteins part of the story. Neither Darwin nor
Mendel knew specifically what genes really were, so either would
have been happy to accept all sorts of inheritable stuff as "genes"
regardless of how it was expressed, and thus would not make *your*
mistake of defining "gene" too narrowly.

Regulatory sequences involved in gene expression are known for a long
time and biology has now probably more definitions of the =93gene=94 than
it really needs. By assuming that =93regulatory sequences=94 or changes in
these sequences may be involved in evolution of morphological traits
you don=92t see it necessary to prove (present evidence) your
assumption. If this is the way the science works, how different is
this from, allow me to borrow your expression, =93(goddiddit because
itpleasedgodtodoit or because itwasgodsplan)?

Regards,

N.C.

.


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