Cell Metabolism, volume 16, issue 1, pages 18-31

Replicative and chronological aging in Saccharomyces cerevisiae.

Valter D. Longo ¹

Gerald S. Shadel ²

Matt Kaeberlein ^{3, 4}

Brian Kennedy ^{4, 5}

Longevity Institute, School of Gerontology, Department of Biological Sciences, and Norris Cancer Center, University of Southern California, 3715 McClintock Avenue, Los Angeles, CA 90089-0191, USA. |

Departments of Pathology and Genetics, Yale University School of Medicine, New Haven, CT 06520-8023, USA |

Department of Pathology, University of Washington, Seattle, WA 98195-7470, USA |

⁴

Institute of Aging Research, Guangdong Medical College, Dongguan 523808, Guangdong, People's Republic of China |

⁵

Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA |

Publication type: Journal Article

Publication date: 2012-07-03

Elsevier

Journal: Cell Metabolism

scimago Q1

wos Q1

SJR: 11.406

CiteScore: 48.6

Impact factor: 27.7

ISSN: 15504131, 19327420

DOI: 10.1016/j.cmet.2012.06.002

Copy DOI

PubMed ID: 22768836

Molecular Biology

Cell Biology

Physiology

Abstract

Saccharomyces cerevisiae has directly or indirectly contributed to the identification of arguably more mammalian genes that affect aging than any other model organism. Aging in yeast is assayed primarily by measurement of replicative or chronological life span. Here, we review the genes and mechanisms implicated in these two aging model systems and key remaining issues that need to be addressed for their optimization. Because of its well-characterized genome that is remarkably amenable to genetic manipulation and high-throughput screening procedures, S. cerevisiae will continue to serve as a leading model organism for studying pathways relevant to human aging and disease.

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