From: Damien Broderick (damien@ariel.ucs.unimelb.edu.au)
Date: Fri Oct 03 1997 - 08:56:34 MDT
At 06:40 PM 10/2/97 -0700, The Willow wrote of my remark that
>} we set out with a limited if
>} Vast immunity repertoire, and the little bastards who breed in us keep
>} changing their formula, so the simple passage of time might [zap us]
>I'm not sure what you're saying here. Considering that we only have
>100,000 active genes, as far as anyone can tell, we start out with a
>rather small immunity repertoire. But lymphocytes -- the antigen
>specific white blood cells -- actually have their genes rearranged as
>they split from a stem cell, thus making them the only somatic cells
>which do not have the same genome as all the other cells. [...] More time
to evolve
>is no inherent advantage on the pathogens side.
Well, I was trying to avoid all the messy details. My key point (borrowing
from William R. Clark's neat little simplified book AT WAR WITHIN, Oxford
UP 1995) is this: the vert immune system is menaced by `a universe of
pathogens that is not only enormous to begin with but full of pathogens
that can alter themselves genetically hundreds of thousands of times faster
than vertebrates can' (263). (Clark has also written a book, which I
haven't seen, appositely entitled SEX AND THE ORIGINS OF DEATH - anyone
read it? Opinions?)
>The entire specific immune system is an excellent example of applied
>evolution
Indeed, although the term `variation' might be preferable since the
`competeing' units are not put through a selection sieve and do not have
descendants as such. The genetic deck shuffling in B cells is a truly cool
gadget, with heavy chain and long chain segments built of randomly combined
V, D and J portions, some 300 fragments in the V pool, 12 D and 6 J,
permitting a basic 20,000 different antibody chains. But because these
segments can be assembled with overlaps, the combinatoire is truly Vast.
Clark again: we thus have a system `for mutating genes that allows you to
create not hundred of *thousands* of new antibodies per *generation*, but
hundreds of *millions*... per hour. Every hour. All life long' (265).
Still, those little critters at the top of the food chain, chewing on us,
do quite often manage to evade the human immune system. I assume that's
due to their stupendous numbers (permitting each species to try lots more
moves than Deep Blue), their rapid generational turnover, and their own
coat-changing. Nesse and Williams, 1995, observe with regard to the
latter: `some pathogens alter their exposed molecular structures so rapidly
that the host has difficulty producing newly needed antibodies fast enough.
This is rapid change without evolution, because the same pathogen genotype
codes for a variety of molecular structures' (EVOLUTION AND HEALING, 63).
But I'm open to correction.
>Homeobox sequences might be conserved not because they get special
>repair mechanisms, but because mutants of those genes thoroughly disable
>their hosts, possibly killing them in development.
Fair enough. But I still have this edgy feeling that some DNA volumes in
the library of Babel have better proofreaders than others - that it's not
just a matter of throwing out any completed copy with the title printed
upside down but of intercepting the bloopers in advance.
>And the whole point is that much DNA is not very highly conserved [...]
>That's how we evolved from prokarya.
That's *not* the *whole* point. It's the most obvious point when the
question is the existence of diversity, but I wanted to direct attention to
the less intuitive islands of stability, and raise the question of how they
managed to remain stationary despite the flux that, incidentally, wears out
our tissues and kills us.
Damien Broderick
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