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Vol. 14, No. 15, pp. 1872-1885, August 1, 2000
Department of Molecular Biology and Pharmacology, Washington
University School of Medicine, St. Louis, Missouri 63110 USA
For a number of organisms, the ability to withstand periods of
nutrient deprivation correlates directly with lifespan. However, the
underlying molecular mechanisms are poorly understood. We show that
deletion of the N-myristoylprotein, Sip2p, reduces resistance to
nutrient deprivation and shortens lifespan in Saccharomyces cerevisiae. This reduced lifespan is due to accelerated aging, as
defined by loss of silencing from telomeres and mating loci, nucleolar
fragmentation, and accumulation of extrachromosomal rDNA. Genetic
studies indicate that sip2
produces its effect on aging by increasing the activity of Snf1p, a
serine/threonine kinase involved in regulating global
cellular responses to glucose starvation. Biochemical analyses reveal
that as yeast age, hexokinase activity increases as does cellular ATP
and NAD+ content. The change in glucose metabolism represents a new
correlate of aging in yeast and occurs to a greater degree, and at
earlier generational ages in sip2 cells. Sip2p
and Snf1p provide new molecular links between the regulation of
cellular energy utilization and aging.
[Key Words: Aging; Saccharomyces cervisiae; N-myristoylproteins; Snf1p kinase interacting protein-2; glucose metabolism; cellular energy storage]
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