The Stationary-Phase Cells of Saccharomyces cerevisiae Display Dynamic Actin Filaments Required for Processes Extending Chronological Life Span

• Published in: Molecular and cellular biology Vol. 35; no. 22; pp. 3892 - 3908
• Main Authors: Vasicova, Pavla, Lejskova, Renata, Malcova, Ivana, Hasek, Jiri
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 01.11.2015; American Society for Microbiology
• Subjects: Actin Cytoskeleton - metabolism; Actin Cytoskeleton - ultrastructure; Actins - metabolism; Actins - ultrastructure; Saccharomyces cerevisiae; Saccharomyces cerevisiae - cytology; Saccharomyces cerevisiae - growth & development; Saccharomyces cerevisiae Proteins - metabolism; Saccharomyces cerevisiae Proteins - ultrastructure
• ISSN: 1098-5549; 0270-7306; 1098-5549
• DOI: 10.1128/MCB.00811-15

Stationary-growth-phase Saccharomyces cerevisiae yeast cultures consist of nondividing cells that undergo chronological aging. For their successful survival, the turnover of proteins and organelles, ensured by autophagy and the activation of mitochondria, is performed. Some of these processes are engaged in by the actin cytoskeleton. In S. cerevisiae stationary-phase cells, F actin has been shown to form static aggregates named actin bodies, subsequently cited to be markers of quiescence. Our in vivo analyses revealed that stationary-phase cultures contain cells with dynamic actin filaments, besides the cells with static actin bodies. The cells with dynamic actin displayed active endocytosis and autophagy and well-developed mitochondrial networks. Even more, stationary-phase cell cultures grown under calorie restriction predominantly contained cells with actin cables, confirming that the presence of actin cables is linked to successful adaptation to stationary phase. Cells with actin bodies were inactive in endocytosis and autophagy and displayed aberrations in mitochondrial networks. Notably, cells of the respiratory activity-deficient cox4Δ strain displayed the same mitochondrial aberrations and actin bodies only. Additionally, our results indicate that mitochondrial dysfunction precedes the formation of actin bodies and the appearance of actin bodies corresponds to decreased cell fitness. We conclude that the F-actin status reflects the extent of damage that arises from exponential growth.