From: BillK (bill@wkidston.freeserve.co.uk)
Date: Wed Apr 02 2003 - 04:06:14 MST
On Wed Apr 02, 2003 12:17 am Anders Sandberg queried:
> Just a quick question to the bright beings on this list: what is the
> opposite of antagonistic pleiotropy? AP is when a gene has a positive
> function in youth and a detrimental in old age. But what do you call a
> gene that does the same thing all the time, but this function is good
> in youth and bad in old age? Is it also called AP? It is the pleiotropy
> part that I am worried about, since the gene does not change behavior
> in any way.
Hmmmm. I suspect that there isn't such a term in use because the
opposite of antagonistic pleiotropy doesn't exist.
There is also discussion that antagonistic pleiotropy itself doesn't
exist either. (See footnote below)
Pleiotropy: One gene leading to many different phenotypic expressions.
An excellent example of a gene with pleiotropic effects is the gene for
myotonic dystrophy. Affected individuals can have one or more of a range
of signs and symptoms including characteristic Christmas-tree like
cataracts, myotonia, narcolepsy, testicular atrophy, frontal balding,
mental retardation, and cardiac abnormalities, among others.
It appears that most genes have pleiotropic effects and the terms
positive and negative pleiotropy are commonly used by researchers.
This is an especial concern for the FDA regarding biotec foods.
FDA regulations assume that pleiotropic effects will not occur when new
genes are inserted into conventional foods such as corn or potatoes or
wheat or soybeans. Therefore, FDA says, genetically modified crops are
"substantially equivalent" to conventional crops.
A key issue is whether "pleiotropic effects" will occur when new genes
are inserted into plants to give the plants desirable new traits.
Pleiotropy means that more than one change occurs in a plant as a result
of the new gene. For example, a gene that allows a plant to grow better
under drought conditions might also make the entire plant grow smaller.
The smaller size would be an unexpected "pleiotropic" effect.
Hope this helps, BillK
---------------------------------------
Reflections on an unsolved problem of biology: the evolution of
senescence and death
William R. Clark, Department of Molecular, Cell and Developmental
Biology, University of California, Los Angeles, California, 90024
ABSTRACT
The evolutionary theory of senescence is based largely on principles
outlined by Williams in 1957, and consists of two relatively independent
parts. The first part builds on ideas first put forward by Medawar,
Haldane and others, to explain how something as negative as senescence
could have been positively selected in evolution, particularly since
most animals in the wild do not reach an age where senescence is
expressed. Williams proposed that the genes responsible for the negative
effects of senecence (senescence effector genes) were fixed in evolution
by a process he called antagonistic pleiotropy, wherein a subset of
genes selected because they confer a reproductive advantage early in
life may have harmful effects in the post-reproductive period; negative
selection against these harmful effects fails because, as pointed out by
Medawar, the force of natural selection declines with age. The
evolutionary history of senescence-causing genes is seen as a
nondirected accumulation of genes selected on a basis independent of
senescence per se. In the second portion of his paper, Williams made a
series of predictions about how the age of organisms at reproductive
maturity, fecundity, lifespan and the timing of the onset of senescence
would all interact in the life history of a species. These latter
predictions, which do not depend at all on details of the mechanisms of
selection of senescence effector genes, have been validated by numerous
experiments over the past several decades. On the other hand, it has
become increasingly evident that the senescence effector genes did not,
as would be predicted by antagonistic pleiotropy, accumulate in a
random, non-directed fashion in various species over evolutionary time.
Rather, everything we know about these genes suggests they were present
in eukaryotic founder cells shortly after, or even congruent with, the
emergence of eukaryotes from their prokaryotic ancestors, and have been
stringently conserved ever since. Complicated explanations of how
so-called "death genes" may have evolved in eukaryotes are thus not
required. It is suggested that the evolutionary theory of senescence
should be focused on those evolutionary principles that have been
validated experimentally, and that the notion of antagonistic pleiotropy
be dropped from theories of the evolution of senescence.
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