Li 2020 G3 (Bethesda)

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Publications in the MiPMap
Li J, Rinnerthaler M, Hartl J, Weber M, Karl T, Breitenbach-Koller H, Mülleder M, Vowinckel J, Marx H, Sauer M, Mattanovich D, Ata Ö, De S, Greslehner GP, Geltinger F, Burhans B, Grant C, Doronina V, Ralser M, Streubel MK, Grabner C, Jarolim S, Moßhammer C, Gourlay CW, Hasek J, Cullen PJ, Liti G, Ralser M, Breitenbach M (2020) Slow growth and increased spontaneous mutation frequency in respiratory deficient afo 1- yeast suppressed by a dominant mutation in ATP3. G3 (Bethesda) [Epub ahead of print].

» PMID: 33093184 Open Access

Li Jing, Rinnerthaler Mark, Hartl Johannes, Weber Manuela, Karl Thomas, Breitenbach-Koller Hannelore, Muelleder Michael, Vowinckel Jakob, Marx Hans, Sauer Michael, Mattanovich Diethard, Ata Oezge, De Sonakshi, Greslehner Gregor P, Geltinger Florian, Burhans Bill, Grant Chris, Doronina Victoria, Ralser Meryem, Streubel Maria Karolin, Grabner Christian, Jarolim Stefanie, Moßhammer Claudia, Gourlay Campbell W, Hasek Jiri, Cullen Paul J, Liti Gianni, Ralser Markus, Breitenbach Michael (2020) G3 (Bethesda)

Abstract: A yeast deletion mutation in the nuclear-encoded gene, AFO1, which codes for a mitochondrial ribosomal protein, led to slow growth on glucose, the inability to grow on glycerol or ethanol, and loss of mitochondrial DNA and respiration. We noticed that afo1- yeast readily obtains secondary mutations that suppress aspects of this phenotype, including its growth defect. We characterized and identified a dominant missense suppressor mutation in the ATP3 gene. Comparing isogenic slowly growing rho-zero and rapidly growing suppressed afo1- strains under carefully controlled fermentation conditions showed that energy charge was not significantly different between strains and was not causal for the observed growth properties. Surprisingly, in a wild-type background, the dominant suppressor allele of ATP3 still allowed respiratory growth but increased the petite frequency. Similarly, a slow-growing respiratory deficient afo1- strain displayed an about twofold increase in spontaneous frequency of point mutations (comparable to the rho-zero strain) while the suppressed strain showed mutation frequency comparable to the repiratory-competent WT strain. We conclude, that phenotypes that result from afo1- are mostly explained by rapidly emerging mutations that compensate for the slow growth that typically follows respiratory deficiency. Keywords: ATP3, Saccharomyces cerevisiae, Growth velocity, Mutation frequency, Rho-zero Bioblast editor: Plangger M O2k-Network Lab: AT Salzburg Breitenbach M, UK Canterbury Gourlay CW


Labels: MiParea: Respiration, mtDNA;mt-genetics, nDNA;cell genetics 


Organism: Saccharomyces cerevisiae 

Preparation: Intact organism 



HRR: Oxygraph-2k 

2020-10