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Yeast apoptosis debate continues

Authors
Journal
The Journal of Cell Biology
0021-9525
Publisher
The Rockefeller University Press
Publication Date
Volume
166
Issue
7
Identifiers
DOI: 10.1083/jcb1667iti1
Keywords
  • News
  • In This Issue

Abstract

untitled Th e Jo ur na l o f C el l B io lo gy 938 The Journal of Cell Biology | Volume 166, Number 7, 2004 In This IssueIn This Issue Yeast apoptosis debate continues east, as a unicellular organism, would seem to benefit most from self-preser- vation. But yeast altruism, in the form of apoptosis, is a new-found, if controversial, field of study. Many doubt the validity of experiments supporting programmed cell death in yeast and call for better controls. In this issue, the debate continues with two new articles that suggest that yeast cells do organize their own deaths—for the sake of their brethren. Biologists often address how a phenom- enon occurs, but seldom why. For the yeast apoptosis field, however, why is a painfully obvious question. On page 1055, Fabrizio et al. suggest a method to the madness. They show that yeast populations survive better in the long run when they initiate an early death program through superoxide. Superoxides are produced by the every- day activities of life, but their mutational and death-inducing activities can be curtailed by superoxide dismutases (Sods). The authors find that Sods are normally down- regulated in older yeast cultures, which are surviving in nutrient-poor medium, leading to cell death. Mutants that circumvented this programmed death mechanism by maintaining high Sod activity had extended life spans. These long-lived populations, however, were unable to repopulate their culture once most of the cells died, a phenomenon known as adaptive regrowth. As a result, in competition experiments, strains that initiated early death eventually outgrew the wild type. Early death probably allows the best- adapted cells in a population to reproduce before they are too old by using nutrients left behind by the dead yeasts. Superoxides are mutation inducers. The higher mutation Y rates that the authors noted in wild-type and other short-lived p

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