NDLI: Sensitivity to Sn2+ of the Yeast Saccharomyces cerevisiae Depends on General Energy Metabolism, Metal Transport, Anti-Oxidative Defences, and DNA Repair

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Sensitivity to Sn2+ of the Yeast Saccharomyces cerevisiae Depends on General Energy Metabolism, Metal Transport, Anti-Oxidative Defences, and DNA Repair

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Sensitivity to Sn2+ of the Yeast Saccharomyces cerevisiae Depends on General Energy Metabolism, Metal Transport, Anti-Oxidative Defences, and DNA Repair

Content Provider	Springer Nature Link
Author	Viau, C. Pungartnik, C. Schmitt, M.C. Basso, T.S. Henriques, J.A.P. Brendel, M.
Copyright Year	2006
Abstract	Resistance to stannous chloride (SnCl2) of the yeast Saccharomyces cerevisiae is a product of several metabolic pathways of this unicellular eukaryote. Sensitivity testing of different null mutants of yeast to SnCl2 revealed that DNA repair contributes to resistance, mainly via recombinational (Rad52p) and error-prone (Rev3p) steps. Independently, the membrane transporter Atr1p/Snq1p (facilitated transport) contributed significantly to Sn2+-resistance whereas absence of ABC export permease Snq2p did not enhance sensitivity. Sensitivity of the superoxide dismutase mutants sod1 and sod2 revealed the importance of these anti-oxidative defence enzymes against Sn2+-imposed DNA damage while a catalase-deficient mutant (ctt1) showed wild type (WT) resistance. Lack of transcription factor Yap1, responsible for the oxidative stress response in yeast, led to 3-fold increase in Sn2+-sensitivity. While loss of mitochondrial DNA did not change the Sn2+-resistance phenotype in any yeast strain, cells with defect cytochrome c oxidase (CcO mutants) showed gradually enhanced sensitivities to Sn2+ and different spontaneous mutation rates. Highest sensitivity to Sn2+ was observed when yeast was in exponential growth phase under glucose repression. During diauxic shift (release from glucose repression) Sn2+-resistance increased several hundred-fold and fully respiring and resting cells were sensitive only at more than 1000-fold exposure dose, i.e. they survived better at 25 mM than exponentially growing cells at 25 μM Sn2+. This phenomenon was observed not only in WT but also in already Sn2+-sensitive rad52 as well as in sod1, sod2 and CcO mutant strains. The impact of metabolic steps in contribution to Sn2+-resistance had the following ranking: Resting WT cells > membrane transporter Snq1p > superoxide dismutases > transcription factor Yap1p ≥ DNA repair $$ \gg $$ exponentially growing WT cells.
Starting Page	705
Ending Page	714
Page Count	10
File Format	PDF
ISSN	09660844
Journal	BioMetals
Volume Number	19
Issue Number	6
e-ISSN	15728773
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	2006-05-12
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	cytochrome oxidase DNA repair genotoxicity glucose repression membrane transport oxidative stress stannous chloride yeast Physical Chemistry Biochemistry
Content Type	Text
Resource Type	Article
Subject	Metals and Alloys Biochemistry, Genetics and Molecular Biology Biomaterials Agricultural and Biological Sciences

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Sensitivity to Sn2+ of the Yeast Saccharomyces cerevisiae Depends on General Energy Metabolism, Metal Transport, Anti-Oxidative Defences, and DNA Repair

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Sensitivity to Sn2+ of the Yeast Saccharomyces cerevisiae Depends on General Energy Metabolism, Metal Transport, Anti-Oxidative Defences, and DNA Repair