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. Author manuscript; available in PMC: 2009 Jul 1.
Published in final edited form as: Biochim Biophys Acta. 2008 Apr 10;1783(7):1280–1285. doi: 10.1016/j.bbamcr.2008.03.017

Figure 1.

Figure 1

Programmed aging and adaptive regrowth in S. cerevisiae. Glucose and nutrients activate the Sch9, Tor1, and Ras/PKA pathways, which in turn promote the down-regulation of Msn2/4/Gis1-dependent stress resistance systems and the production of superoxide. High levels of superoxide damage the mitochondria causing aging and apoptosis. Additionally, superoxide causes DNA damage and increases DNA mutations. Cell death leads to the release of nutrients that are utilized by “regrowth” mutants to reenter the cell cycle. Cytochrome C released from the mitochondria may function to signal apoptotic death. Ethanol, accumulated during exponential growth, is also involved in the activation of programmed aging.