Re: Opposite of antagonistic pleiotropy

From: BillK (bill@wkidston.freeserve.co.uk)
Date: Wed Apr 02 2003 - 04:06:14 MST

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    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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