The role of K+ and H+ transport systems during glucose- and H2O2-induced cell death in Saccharomyces cerevisiae
Autor: | Jorge Pérez-Valle, Guillem Hueso, José M. Mulet, Sukesh Chander Sharma, María D. Planes, Lynne Yenush, Frank A. Hoeberichts, Consuelo Montesinos, Ramón Serrano |
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Rok vydání: | 2010 |
Předmět: |
Programmed cell death
Saccharomyces cerevisiae Proteins Saccharomyces cerevisiae Bioengineering Vacuole Applied Microbiology and Biotechnology Biochemistry H(+)-K(+)-Exchanging ATPase Osmotic Pressure Genetics Cation Transport Proteins Caspase Membrane potential Cell Death biology Hydrogen Peroxide biology.organism_classification Cell biology Cytolysis Cytosol Glucose Potassium biology.protein Efflux Reactive Oxygen Species Hydrogen Biotechnology |
Zdroj: | Yeast. 27:713-725 |
ISSN: | 0749-503X |
DOI: | 10.1002/yea.1767 |
Popis: | Glucose, in the absence of additional nutrients, induces programmed cell death in yeast. This phenomenon is independent of yeast metacaspase (Mca1/Yca1) and of calcineurin, requires ROS production and it is concomitant with loss of cellular K+ and vacuolar collapse. K+ is a key nutrient protecting the cells and this effect depends on the Trk1 uptake system and is associated with reduced ROS production. Mutants with decreased activity of plasma membrane H+-ATPase are more tolerant to glucose-induced cell death and exhibit less ROS production. A triple mutant ena1-4 tok1 nha1, devoid of K+ efflux systems, is more tolerant to both glucose- and H2O2-induced cell death. We hypothesize that ROS production, activated by glucose and H+-ATPase and inhibited by K+ uptake, triggers leakage of K+, a process favoured by K+ efflux systems. Loss of cytosolic K+ probably causes osmotic lysis of vacuoles. The nature of the ROS-producing system sensitive to K+ and H+ transport is unknown. Copyright © 2010 John Wiley & Sons, Ltd. |
Databáze: | OpenAIRE |
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