TIMES item on speciation
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- Date: Wed, 25 Nov 1998 01:30:48 -0800 (PST)
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This describes current research. To me this piece provides
a clue that a new GM species may have an in-built inability to
spread into existing populations.
Is this a realistic "hope" as far as plant species are concerned, or does
the piece also imply that in-built inability to spread may also be removed
by GE ?
London Times November 25 1998
Science Briefing: Nigel Hawkes
Darwin's hidden secrets
CHARLES DARWIN may have called his masterpiece The Origin of Species,
but it actually says little about that subject. He explains how
individual species evolve, but not how new species originate. This
process, known as speciation, remains deeply puzzling even today,
despite the huge growth of knowledge about molecular genetics.
Geographical isolation and a change in the environment are two factors
that favour speciation, but they hardly seem adequate to trigger it.
Now two teams, one from Scripps Institution of Oceanography in La
Jolla, California, and the other from the University of Chicago, have
identified genes that could control the process.
The Chicago team, led by Professor Chung-I Wu, started from the
observation that matings between closely related species - the horse
and the donkey, for example - often produce offspring that are
sterile. Male sterility appears to be a barrier that keeps species
Using fruit flies, Professor Wu and colleagues searched for the genes
responsible. They took progressively shorter pieces of DNA from one
species, Drosophila simulans, and introduced them into another,
Drosophila mauritania. They knew that the gene they wanted must lie
between the shortest insert that caused infertility and the longest
that did not.
In the current issue of Science they report that the gene they found,
called Odysseus, lies on a piece of DNA that hardly changes between
species. These so-called homeobox genes, which are involved in shaping
the embryo and controlling development of its cells, are among the
slowest-evolving of all genes.
"Homeobox genes usually don't differ by more than a few base pairs,
even when you compare them in humans and invertebrates," says
Professor Wu. "But when we looked at this homeobox gene in two very
closely related species of fruit fly, they were extremely different,
suggesting that the gene is evolving at a highly accelerated rate."
He estimates that it is changing up to 1,000 times faster than any
other homeobox gene studied.
The reason, he believes, is that it controls male sexual function, and
rapid changes in such genes would be favoured because they might give
one male the edge in the struggle to fertilise females. But the rapid
change also means that one male's DNA may alter so quickly that it can
no longer work when combined with the DNA of a female which has not
changed. In this case, the two can produce offspring, but the males
are sterile, so the line comes to an abrupt end.
Similar rapid evolution lies behind another model of speciation, from
Dr Willie Swanson and Dr Victor Vacquier of Scripps, published in
Science in July. They show that in the abalone - a mollusc - the sperm
produce a protein, lysin, which creates a hole in the egg envelope to
enable fertilisation to occur. Lysin has to lock on to a receptor on
the egg for this to occur, and the gene for that receptor can change
rapidly, just like Odysseus.
The chances are that other genes are also involved. But it looks as if
the secrets hidden to Darwin are at last beginning to be unlocked.