Increasing Saccharomyces cerevisiae stress resistance, through the overactivation of the heat shock response resulting from defects in the Hsp90 chaperone, does not extend replicative life span but can be associated with slower chronological ageing of nondividing cells
N. Harris et al., Increasing Saccharomyces cerevisiae stress resistance, through the overactivation of the heat shock response resulting from defects in the Hsp90 chaperone, does not extend replicative life span but can be associated with slower chronological ageing of nondividing cells, MOL GENET G, 265(2), 2001, pp. 258-263
Recent studies on Drosophila and Caenorhabditis elegans indicate that incre
ases in stress resistance result in a longer chronological life span, an ef
fect that must operate primarily on the postmitotic tissues of the adult. S
tress resistance can be increased through decreases In Hsp90 chaperone acti
vity, since Hsp90 acts to downregulate the activity of heat shock transcrip
tion factor. This study investigated whether the increases in stress resist
ance associated with reduced Hsp90 chaperone activity influence ageing in t
he budding yeast Saccharomyces cerevisiae, ageing being measured either as
the replicative (nonchronological) senescence of budding cells or as the ch
ronological ageing of non-dividing (stationary phase) cultures. Overactivat
ion of the heat shock response caused no slowing of replicative senescence.
In some situations though it was associated with a longer chronological li
fe span of stationary cells, the yeast equivalent of the postmitotic state.
This is consistent With the idea that stress resistance exerts its life sp
an-extending effects primarily in postmitotic cells and tissues.