Physiological scenarios of programmed loss of mitochondrial DNA function and death of yeast

• Published in: Biochemistry (Moscow) Vol. 76; no. 2; pp. 167 - 171
• Main Authors: Kochmak, S. A., Knorre, D. A., Sokolov, S. S., Severin, F. F.
• Format: Journal Article
• Language: English
• Published: Dordrecht SP MAIK Nauka/Interperiodica 01-02-2011; Springer; Springer Nature B.V
• Subjects: Aging; Apoptosis; Apoptosis - physiology; Biochemistry; Biomedical and Life Sciences; Biomedicine; Bioorganic Chemistry; Cell Division; Culture Media - metabolism; DNA Damage; DNA, Mitochondrial - metabolism; Life Sciences; Microbiology; Mitochondria - metabolism; Mitochondrial DNA; Mortality; Physiological aspects; Physiology; Proton-Translocating ATPases; Quorum Sensing - physiology; Reactive Oxygen Species - metabolism; Review; Saccharomyces cerevisiae; Saccharomyces cerevisiae - cytology; Saccharomyces cerevisiae - physiology; Suicide; Yeast; Yeasts; apoptosis; aging; mitochondria; yeast; petite
• ISSN: 0006-2979; 1608-3040
• DOI: 10.1134/S0006297911020015

Recently it was convincingly shown that the yeast
Saccharomyces cerevisiae
does possess the basic modules of programmed cell death machinery. As programmed cell death is suicide for a unicellular organism, it is reasonable to assume that they trigger the program when the death is beneficial for the rest of the population. Not surprisingly, most of the scenarios of physiological death of
S. cerevisiae
, i.e. cell death in stationary culture, during meiosis, during mating, and driven by viruses are dependent on quorum sensing, meaning that they depend on the cell density. Here we also discuss possible mechanisms that govern fitness decline during replicative aging of
S. cerevisiae
cells. We argue that loss of mitochondrial DNA function that occurs during replicative aging is programmed and adaptive. Indeed, yeast cells with nonfunctional mitochondrial DNA are known to be extremely stress-resistant, and also the presence of a subpopulation of such cells might protect the culture from degeneration by preventing the fixation of opportunistic mutations.