X-Message-Number: 25722
Date: Thu, 24 Feb 2005 05:22:36 -0800 (PST)
From: Doug Skrecky <>
Subject: Superoxide probably not a major driver of fly senescence

Aging Cell. 2003 Apr;2(2):123-30
Testing an 'aging gene' in long-lived drosophila strains: increased
longevity depends on sex and genetic background.
  Molecular advances of the past decade have led to the discovery of a
myriad of 'aging genes' (methuselah, Indy, InR, Chico, superoxide
dismutase) that extend Drosophila lifespan by up to 85%. Despite this
life extension, these mutants are no longer lived than at least some
recently wild-caught strains. Typically, long-lived mutants are identified
in relatively short-lived genetic backgrounds, and their effects are
rarely tested in genetic backgrounds other than the one in which they
were isolated or derived. However, the mutant's high-longevity phenotype
may be dependent on interactions with alleles that are common in
short-lived laboratory strains. Here we set out to determine whether one
particular mutant could extend lifespan in long-lived genetic backgrounds
in the fruit fly, Drosophila melanogaster. We measured longevity and
resistance to thermal stress in flies that were transgenically altered to
overexpress human superoxide dismutase (SOD) in the motorneurones in each
of 10 genotypes. Each genotype carried the genetic background from a
different naturally long-lived wild-caught Drosophila strain. While SOD
increased lifespan on average, the effect was genotype- and
sex-specific. Our results indicate that naturally segregating genes
interact epistatically with the aging gene superoxide dismutase to modify
its ability to extend longevity. This study points to the need to
identify mutants that increase longevity not only in the lab strain of
origin but also in naturally long-lived genetic backgrounds.

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