Reference: Hoeberichts FA, et al. (2010) The role of K(+) and H(+) transport systems during glucose- and H(2)O(2)-induced cell death in Saccharomyces cerevisiae. Yeast 27(9):713-25

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Abstract

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 H(2)O(2)-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 (c) 2010 John Wiley & Sons, Ltd.

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Journal Article
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Hoeberichts FA, Perez-Valle J, Montesinos C, Mulet JM, Planes MD, Hueso G, Yenush L, Sharma SC, Serrano R
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