Slow Growth and Increased Spontaneous Mutation Frequency in Respiratory Deficient afo1- Yeast Suppressed by a Dominant Mutation in ATP3. Issue 12 (1st December 2020)

• Record Type: Journal Article
• Authors: Li, Jing; Rinnerthaler, Mark; Hartl, Johannes; Weber, Manuela; Karl, Thomas; Breitenbach-Koller, Hannelore; Mülleder, Michael; Vowinckel, Jakob; Marx, Hans; Sauer, Michael; Mattanovich, Diethard; Ata, Özge; 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
• Is Part Of: G3. Volume 10:Issue 12(2020)
• Page Start: 4637
• Page End: 4648
• Publication Date: 2020-12-01
• Subjects: Saccharomyces cerevisiae -- rho-zero -- growth velocity -- mutation frequency -- ATP3; Genetics -- Research -- Periodicals; Genomics -- Periodicals; Genetics; Genomics; Genes; Genetics -- Research; Genomics; Electronic journals; Periodical; Periodicals; Fulltext; Internet Resources; Periodicals; 572.8
• DOI: 10.1534/g3.120.401537
• Languages: English
• ISSNs: 2160-1836

Abstract

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 respiratory-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.