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Updated: Apr 21, 2026

Quantifying Yeast Chronological Life Span by Outgrowth of Aged Cells
Published on: May 5, 2009
Mitochondria, reactive oxygen species, and chronological aging: a message from yeast
1Gladstone Institute of Virology and Immunology, University of California-San Francisco, 1650 Owens Street, San Francisco, CA 94158, United States. yong.pan@gladstone.ucsf.edu
Abstract:
As a major intracellular source of reactive oxygen species (ROS), mitochondria are involved in aging and lifespan regulation. Using the yeast chronological aging model, researchers have identified conserved signaling pathways that affect lifespan by modulating mitochondrial functions. Caloric restriction and a genetic mimetic with reduced target of rapamycin signaling globally upregulate the mitochondrial proteome and respiratory functions. Recent discoveries support the notion that an altered mitochondrial proteome induces mitohormesis. Mitohormesis involves a variety of ROS during several growth stages and extends lifespan in yeast and other organisms. Here we recap recent advances in understanding of ROS as signals that decelerate chronological aging in yeast. We also discuss parallels between yeast and worm hypoxic signaling. In sum, this mini-review covers mitochondrial regulation by nutrient-sensing pathways and the complex underlying interactions of ROS, metabolic pathways, and chronological aging.
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