SETI public: Fw: Cornell News: rapid evolution

From: LARRY KLAES (ljk4_at_msn.com)
Date: Wed Jul 16 2003 - 14:16:30 PDT

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    ----- Original Message -----
    From: cunews_at_cornell.edu
    Sent: Wednesday, July 16, 2003 5:03 PM
    To: CUNEWS-LIFE_SCIENCE-L_at_cornell.edu; CUNEWS-SCIENCE-L_at_cornell.edu
    Subject: Cornell News: rapid evolution

    Evolutionary 'fast-track,' in which the hunted outwit their hunters,
    could explain why human diseases progress so rapidly, Cornell
    biologists report

    HOLD FOR EMBARGO: Wednesday, July 16, 2003, 1 p.m. EDT

    Contact: Roger Segelken
    Office: 607-255-9736
    E-mail: hrs2_at_cornell.edu

    ITHACA, N.Y. -- In the fishbowl of life, when hordes of well-fed
    predators drive their prey to the brink of extinction, sometimes
    evolution takes the fast track to help the hunted survive -- and then
    thrive to outnumber their predators.

    This rapid evolution, predicted by Cornell University biologists in
    computer models and demonstrated with Pac-Man-like creatures and
    their algae food in laboratory habitats called chemostats, could play
    an important role in the ecological dynamics of many predator-prey
    systems, according to an article in the latest issue (July 17, 2003)
    of the journal Nature.

    Physicians, the Cornell biologists say, should keep this rapid
    evolution in mind when investigating interactions between diseases
    and victims. As one example, they say, it is useful in trying to
    understand how HIV, the AIDS virus, manages to evolve so swiftly that
    development of improved vaccines is extremely difficult.

    "Evolution is not just about dinosaurs and apes, but it can occur
    much more rapidly than we previously thought. Rapid evolution is
    pervasive, and the list of examples is growing," says Takehito
    Yoshida, a postdoctoral research fellow in Cornell's Department of
    Ecology and Evolutionary Biology and lead author of the Nature
    article. Yoshida demonstrated the evolutionary principle with
    near-microscopic, multicelled animals called rotifers that live to
    gobble much tinier green algae. He notes, "We humans are part of
    complex ecosystems, and if we think we're above the effects of
    evolution, we're not looking close enough. If we want to understand
    epidemics and outbreaks of insects such as gypsy moths, we should not
    ignore the effect of evolution."

    Other Cornell authors of the Nature report, illustrated with a cover
    photo of a rotifer-eating algae and the headline "Fast Food," are
    Laura E. Jones, a postdoctoral researcher, and Stephen P. Ellner, a
    professor of ecology and evolutionary biology, who conducted computer
    modeling of predator-prey dynamics; Gregor F. Fussmann, a
    postdoctoral researcher during the experiments and now a biologist at
    the University of Potsdam, Germany; and Nelson G. Hairston Jr.,
    professor of ecology and evolutionary biology. The studies were
    supported by a grant from the Mellon Foundation.

    The rotifers, Brachionas calyciflorus, and the algae, Chlorella
    vulgaris, were chosen for the experiment because they are the
    standard, well-documented "lab rats of freshwater predator-prey
    studies," Hairston says. The eaters and the eaten lived together for
    months in transparent glass chemostats stocked with nutrients (for
    the algae) and water.

    The Hairston research group had noticed that the highs and lows of
    predator and prey populations in the chemostats were occurring
    completely "out of phase," says Yoshida. When rotifer populations
    were very high -- because previously they had plenty of algae to eat,
    algal populations hit rock bottom, because they had been consumed
    almost out of existence. The opposite occurred when algae were
    super-abundant: There were almost no rotifers around to eat them.
    Hairston and his collaborators were seeing weeks go by between the
    very pronounced oscillations in predator and prey populations.

    Computer models developed by Ellner and graduate student Kyle
    Shertzer predicted that only evolution on the part of the prey could
    account for the out-of-phase, prolonged oscillation effect. Jones and
    Ellner refined the models to make detailed predictions about the
    effects of prey evolution, and Yoshida and Fussmann ran experiments
    in chemostats under two kinds of conditions: In one, all the
    single-cell algae were genetically identical clones -- essentially
    one-trick ponies that could not evolve their way out of a tough
    situation; in the second, the algal population was genetically varied
    so that somewhere among their tiny green gene pool might be an
    evolutionary innovation or two that could save them.

    After running the chemostats for months and counting predator and
    prey populations day by day, the computer model's prediction proved
    correct. Populations of a single algal clone quickly rose and fell
    almost in synchrony with the numbers of rotifers. But the algae with
    some genetic variation to draw on enjoyed longer periods when they
    were abundant and their predators were few -- along with agonizingly
    long periods when they struggled to rebuild their populations.

    Instead of millions of years, the algae were evolving in a few weeks.
    But exactly how had they changed?

    "We're not sure," Hairston says. "We think that somehow they made
    themselves indigestible. They figured out how to pass straight
    through the rotifer gut without being digested and survived to make
    lots more of themselves. Rapid evolution got them out of a tight
    spot."

    In one respect the joke is on the fast-evolving algae, Hairston
    notes, because they had to give up something to become indigestible:
    They became slow-growing algae relative to their kin. As a result,
    the next time they compete for food resources, the slow-growing,
    hard-to-eat algae will be at a disadvantage, and the more edible
    algae will thrive, allowing the cycle to repeat indefinitely.

    Ellner suggests that this cycle of rapid evolution -- between defense
    and vulnerability -- could have parallels in human diseases. "There's
    hardly anyone left in our [human] population who had resistance or
    developed it during the 1918 flu epidemic," he says. "Perhaps the
    time is now ripe for a return of those strains or their relatives."

    Jones sees some hope that medical researchers will come to recognize
    the role of rapid evolution. "HIV is evolving so quickly that
    researchers are struggling to make an effective vaccine. As we say in
    our report, evolution can substantially alter predator-prey dynamics.
    Attempts to understand population oscillations cannot afford to
    neglect the potential effects of ongoing, rapid evolution."

    -30-

    The web version of this release, with accompanying photos, may be
    found at
    http://www.news.cornell.edu/releases/July03/rapid.evolution.hrs.html

    Cornell University News Service
    Surge 3
    Cornell University
    Ithaca, NY 14853
    607-255-4206
    cunews_at_cornell.edu
    http://www.news.cornell.edu


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