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J. Biol. Chem., Vol. 269, Issue 28, 18638-18645, Jul, 1994
J Sun, SP Kale, AM Childress, C Pinswasdi and SM Jazwinski
Individual cells of the yeast Saccharomyces cerevisiae have a limited
replicative life-span. The role of the genes RAS1 and RAS2 in yeast
longevity was examined. Over-expression of RAS2 led to a 30% increase in
the life-span on average and postponed the senescence-related increase in
generation time seen during yeast aging. No life-span extension was
obtained by overexpression of RAS1. However, deletion of RAS1 prolonged the
life-span. These results suggest that RAS1 and RAS2 play reciprocal roles
in determining yeast longevity. RAS1 and RAS2 mRNA and protein levels
declined with replicative age, suggesting a diminishing impact on yeast
longevity. The major known pathway through which Ras proteins function in
yeast involves stimulation of adenylate cyclase. No evidence for a
life-span-extending effect of elevated intracellular cAMP was found.
Indeed, high intracellular cAMP was associated with curtailed life-span. A
similar decrease in life-span was found on disruption of BCY1, which codes
for the regulatory subunit of protein kinase A, the downstream target of
cAMP. Importantly, overexpression of an effector domain mutant of RAS2,
defective in stimulation of adenylate cyclase, prolonged life-span to the
same extent as the wild-type gene, suggesting that the cAMP pathway is
neither sufficient nor necessary for increased longevity.
Divergent roles of RAS1 and RAS2 in yeast longevity
Department of Biochemistry and Molecular Biology, Louisiana State University Medical Center, New Orleans 70112.
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