Re: Darwin, Evolution, the Animal Kingdom, and Man

From: Michael Olea (oleaj_at_sbcglobal.net)
Date: 12/06/04


Date: Mon, 06 Dec 2004 05:17:39 GMT

in article oJ%rd.27156$kI6.1506597@news20.bellglobal.com, Wolf Kirchmeir at
wwolfkir@sympatico.ca wrote on 12/3/04 7:37 AM:

> Lester Zick wrote:
> [...]
>>
>> I find myself wondering if there are any biological evolutionary
>> mechanisms other than random mutation mechanisms of natural selection?

>>
>> Regards - Lester
>
>
> Don't wonder, read. You'd find out, eg, that the expression of genes
> depends on the organisms' environment, which means that inactive "legacy
> genes" may become active when the environment changes. ...

True, and interesting, but not germain - environmentaly triggered changes in
gene *expression* do not change heritable genetic material (which would
constitute inheritance of acquired characteristics) - the same DNA is passed
on. No evolution has taken place. Of course environmental influences (e.g.
high levels of radiation) can trigger mutations, but these are in no way
directed: "There appears to be no way in which changes in the environment
can call forth specific gene mutations. No matter how pressing the need,
change must wait upon chance mutations" (Harold, The Way Of The Cell).

> ... Contrarywise, a
> stable environment tends to prevent evolutionary change, since mutations
> are more likely not to have a beneficial effect; but some mutations
> survive because they have no effect, and may come into play when the
> environment changes; and so on. Or that genetic drift is a powerful
> weeder-out of genes, some of which might have enabled an organism to
> survive environmental changes.

Here you are pointing to the role of the environment in *selecting* changes
that nevertheless arise as random mutations.

> ... Or the fact that most genes code for only
> part of a protein, and that genes must be cut and pasted to make the the
> sequence that produces a particular protein.

One man one vote, one gene one protein. I wonder if what you are really
talking about here is exons and introns - stretches of coding and non-coding
DNA in eukaryotic genomes. Introns are removed from the messenger RNA
transcribed from DNA. So in effect exons are stiched together to make the
RNA that serves as the template for a particular protein. There is, however,
another form of cut and paste - alternative splicing of pieces of a gene - a
set of altertnative exons any one of which ends up in the transcribed mRNA.
So in this case one gene codes for many proteins.

But it is a matter of convention what you want to call a gene: "Crudely
speaking, one gene codes for one protein, but there are so many exceptions
to this statement that the term does not have an agreed formal meaning in
biology any more" (Ridley, The Cooperative Gene).

Here I started to launch into a digression on start and stop codons, "open
reading frames", and the use of hidden markov models, neural nets, support
vector machines, and the like in programs like "genefinder" - interesting
stuff, at least to me, but peripheral to the question. So, aside from this
note, that discussion has been excised by CAP digreserase.

> ... That's important because
> the cutters and pasters are RNA molecules, which are more likely to
> respond to environmental inputs that DNA molecules; which in turn means
> that environment can cause changes in the organism, albeit in a very
> roundabout way. ...

But again you are talking about gene expression - the environment in this
scenario is not causing *heritable* changes in the organism.

> ... Or that bacteria appear to have a mechanism that
> rnadomly rearranges DNA, which appears to be a major factor in the
> development of antibiotic resistance. ...

Now this is interesting - could a bacterium thus bootstrap its fitness in a
way analogous to the way e. coli swims upgradient towards a chemical
attractant (chemotaxis - by alternating runs, which carry e. coli in a
particular direction, with tumbles, which send it off in a random new
direction, long runs as long as it is moving up-gradient, short runs when it
moves down gradient, e. coli manages to wander up a gradient)? Fitnotaxis?

Well, no - it could not, on second thought. Initiating random rearangement
of DNA is a little like a tumble, but there is no analog of a run - it is
more like an act of desperation - like deciding one's position in fitness
space is so bad that any change is apt to lead to a better place. Such a
"decision" would of course have to have some biochemical basis - some
molecular cascade that in effect monitors "fitness" (am I getting enough,
uh, aspartate, do I have any hope of achieving the ultimate cellular dream -
e unum pluribus?) and at some threshold (I am so down everything looks like
up to me) takes the plunge.

But this is still random mutation, as you describe it, though directed in
the sense that it would seem to be initiated in response to environmental
factors.

> ... And so on. It's much more
> complicated than random genetic mutation. {Any errors in the above are
> my own.}

The only agent of evolutionary change you have pointed to is random genetic
mutation.

>
> Bottom line: evolution is the effect of the interaction between genes
> and environment. Neither can work withouit the other.

Perhaps there are mechanisms other than natural selection of random
mutations also at work in evolution - lateral gene transfer, say - the
mergers of symbiots with hosts (mitochondira, chlorplasts...), or bacterial
"sex", but you have not made the case. You have pointed to the complex
interplay between gene expression and environment - fascinating stuff
certainly, but it does not address the issue - not unless you can show
inheritance of acquired characteristics



Relevant Pages

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  • News: Darwins children.
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