Abstract

Chronological life span is defined by how long a cell can survive in a non-dividing state. In yeast, it is measured by viability after entry into stationary phase. To date, some factors affecting chronological life span have been identified; however, the molecular details of how these factors regulate chronological life span have not yet been elucidated clearly. Because life span is a complicated phenomenon and is supposedly regulated by many factors, it is necessary to identify new factors affecting chronological life span to understand life span regulation. To this end, we have screened for long-lived mutants and identified Pma1, an essential P-type proton ATPase, as one of the determinants of chronological life span. We show that partial loss of Pma1 activity not only by mutations but also by treatment with the Pma1 inhibitory chemical vanadate resulted in the long-lived phenotype in Schizosaccharomyces pombe. These findings suggest a novel way to manipulate chronological life span by modulating Pma1 as a molecular target.

Highlights

  • In Saccharomyces cerevisiae, two of the major pathways that control chronological life span have been identified: the RasPKA-Msn2/4 pathway and the Sch9 pathway (3, 4)

  • On the basis of these observations, we proposed that Ecl1 family proteins are novel regulators for chronological life span in yeast

  • Because life span is supposed to be regulated by many factors and complicatedly and important factors for life span regulation have been conserved in eukaryotes, it is necessary to identify new conserved factors affecting chronological life span to understand life span regulation (13)

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Summary

Introduction

In Saccharomyces cerevisiae, two of the major pathways that control chronological life span have been identified: the RasPKA-Msn2/4 pathway and the Sch9 pathway (3, 4). The period in which the cells keep their viability after entry into stationary phase is recognized as the chronological life span (2). In Schizosaccharomyces pombe, Pka1 and Sck2 are regulators of chronological life span; each mutant shows a long-lived phe-

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