NDLI: Yeast colony survival depends on metabolic adaptation and cell differentiation rather than on stress defense.

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Yeast colony survival depends on metabolic adaptation and cell differentiation rather than on stress defense.

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Yeast colony survival depends on metabolic adaptation and cell differentiation rather than on stress defense.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cáp, Michal Váchová, Libuse Palková, Zdena
Description	Author Affiliation: Cáp M ( Department of Genetics and Microbiology, Faculty of Sciences, Charles University in Prague, Vinicná 5, 128 44 Prague 2, Czech Republic.)
Abstract	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.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	47
Volume Number	284
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2009-11-20
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Saccharomyces Cerevisiae Physiology Ammonia Metabolism Catalase Cytosol Epigenesis, Genetic Genes, Fungal Glutamate-Ammonia Ligase Glutathione Peroxidase Mitochondria Models, Biological Mutation Oxidative Stress Reactive Oxygen Species Saccharomyces Cerevisiae Proteins Signal Transduction Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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