Yeast colony survival depends on metabolic adaptation and cell differentiation rather than on stress defense
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
Grant support
55005623
Howard Hughes Medical Institute - United States
PubMed
19801643
PubMed Central
PMC2781671
DOI
10.1074/jbc.m109.022871
PII: S0021-9258(20)37848-0
Knihovny.cz E-resources
- MeSH
- Ammonia metabolism MeSH
- Models, Biological MeSH
- Cytosol metabolism MeSH
- Epigenesis, Genetic MeSH
- Genes, Fungal MeSH
- Glutamate-Ammonia Ligase metabolism MeSH
- Glutathione Peroxidase metabolism MeSH
- Catalase metabolism MeSH
- Mitochondria metabolism MeSH
- Mutation MeSH
- Oxidative Stress MeSH
- Reactive Oxygen Species MeSH
- Saccharomyces cerevisiae Proteins metabolism MeSH
- Saccharomyces cerevisiae metabolism physiology MeSH
- Signal Transduction MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Ammonia MeSH
- Glutamate-Ammonia Ligase MeSH
- Glutathione Peroxidase MeSH
- Catalase MeSH
- Reactive Oxygen Species MeSH
- Saccharomyces cerevisiae Proteins MeSH
Enzymes scavenging reactive oxygen species (ROS) are important for cell protection during stress and aging. A deficiency in these enzymes leads to ROS imbalance, causing various disorders in many organisms, including yeast. In contrast to liquid cultures, where fitness of the yeast population depends on its ROS scavenging capability, the present study suggests that Saccharomyces cerevisiae cells growing in colonies capable of ammonia signaling use a broader protective strategy. Instead of maintaining high levels of antioxidant enzymes for ROS detoxification, colonies activate an alternative metabolism that prevents ROS production. Colonies of the strain deficient in cytosolic superoxide dismutase Sod1p thus developed the same way as wild type colonies. They produced comparable levels of ammonia and underwent similar developmental changes (expression of genes of alternative metabolism and center margin differentiation in ROS production, cell death occurrence, and activities of stress defense enzymes) and did not accumulate stress-resistant suppressants. An absence of cytosolic catalase Ctt1p, however, brought colonies developmental problems, which were even more prominent in the absence of mitochondrial Sod2p. sod2Delta and ctt1Delta colonies failed in ammonia production and sufficient activation of the alternative metabolism and were incapable of center margin differentiation, but they did not increase ROS levels. These new data indicate that colony disorders are not accompanied by ROS burst but could be a consequence of metabolic defects, which, however, could be elicited by imbalance in ROS produced in early developmental phases. Sod2p and homeostasis of ROS may participate in regulatory events leading to ammonia signaling.
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