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Heat stress-induced life span extension in yeast.
Exp Cell Res. 1998 Dec 15; 245(2):379-88.EC

Abstract

The yeast Saccharomyces cerevisiae has a limited life span that can be measured by the number of times individual cells divide. Several genetic manipulations have been shown to prolong the yeast life span. However, environmental effects that extend longevity have been largely ignored. We have found that mild, nonlethal heat stress extended yeast life span when it was administered transiently early in life. The increased longevity was due to a reduction in the mortality rate that persisted over many cell divisions (generations) but was not permanent. The genes RAS1 and RAS2 were necessary to observe this effect of heat stress. The RAS2 gene is consistently required for maintenance of life span when heat stress is chronic or in its extension when heat stress is transient or absent altogether. RAS1, on the other hand, appears to have a role in signaling life extension induced by transient, mild heat stress, which is distinct from its life-span-curtailing effect in the absence of stress and its lack of involvement in the response to chronic heat stress. This distinction between the RAS genes may be partially related to their different effects on growth-promoting genes and stress-responsive genes. The ras2 mutation clearly hindered resumption of growth and recovery from stress, while the ras1 mutation did not. The HSP104 gene, which is largely responsible for induced thermotolerance in yeast, was necessary for life extension induced by transient heat stress. An interaction between mitochondrial petite mutations and heat stress was found, suggesting that mitochondria may be necessary for life extension by transient heat stress. The results raise the possibility that the RAS genes and mitochondria may play a role in the epigenetic inheritance of reduced mortality rate afforded by transient, mild heat stress.

Authors+Show Affiliations

Department of Biochemistry and Molecular Biology, Louisiana State University Medical Center, New Orleans, Louisiana, 70112, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9851879

Citation

Shama, S, et al. "Heat Stress-induced Life Span Extension in Yeast." Experimental Cell Research, vol. 245, no. 2, 1998, pp. 379-88.
Shama S, Lai CY, Antoniazzi JM, et al. Heat stress-induced life span extension in yeast. Exp Cell Res. 1998;245(2):379-88.
Shama, S., Lai, C. Y., Antoniazzi, J. M., Jiang, J. C., & Jazwinski, S. M. (1998). Heat stress-induced life span extension in yeast. Experimental Cell Research, 245(2), 379-88.
Shama S, et al. Heat Stress-induced Life Span Extension in Yeast. Exp Cell Res. 1998 Dec 15;245(2):379-88. PubMed PMID: 9851879.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Heat stress-induced life span extension in yeast. AU - Shama,S, AU - Lai,C Y, AU - Antoniazzi,J M, AU - Jiang,J C, AU - Jazwinski,S M, PY - 1998/12/16/pubmed PY - 1998/12/16/medline PY - 1998/12/16/entrez SP - 379 EP - 88 JF - Experimental cell research JO - Exp Cell Res VL - 245 IS - 2 N2 - The yeast Saccharomyces cerevisiae has a limited life span that can be measured by the number of times individual cells divide. Several genetic manipulations have been shown to prolong the yeast life span. However, environmental effects that extend longevity have been largely ignored. We have found that mild, nonlethal heat stress extended yeast life span when it was administered transiently early in life. The increased longevity was due to a reduction in the mortality rate that persisted over many cell divisions (generations) but was not permanent. The genes RAS1 and RAS2 were necessary to observe this effect of heat stress. The RAS2 gene is consistently required for maintenance of life span when heat stress is chronic or in its extension when heat stress is transient or absent altogether. RAS1, on the other hand, appears to have a role in signaling life extension induced by transient, mild heat stress, which is distinct from its life-span-curtailing effect in the absence of stress and its lack of involvement in the response to chronic heat stress. This distinction between the RAS genes may be partially related to their different effects on growth-promoting genes and stress-responsive genes. The ras2 mutation clearly hindered resumption of growth and recovery from stress, while the ras1 mutation did not. The HSP104 gene, which is largely responsible for induced thermotolerance in yeast, was necessary for life extension induced by transient heat stress. An interaction between mitochondrial petite mutations and heat stress was found, suggesting that mitochondria may be necessary for life extension by transient heat stress. The results raise the possibility that the RAS genes and mitochondria may play a role in the epigenetic inheritance of reduced mortality rate afforded by transient, mild heat stress. SN - 0014-4827 UR - https://www.unboundmedicine.com/medline/citation/9851879/Heat_stress_induced_life_span_extension_in_yeast_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4827(98)94279-3 DB - PRIME DP - Unbound Medicine ER -