RT Journal Article SR Electronic T1 Slow Growth and Increased Spontaneous Mutation Frequency in Respiratory Deficient afo1- Yeast Suppressed by a Dominant Mutation in ATP3 JF G3: Genes|Genomes|Genetics FD Genetics Society of America SP 4637 OP 4648 DO 10.1534/g3.120.401537 VO 10 IS 12 A1 Li, Jing A1 Rinnerthaler, Mark A1 Hartl, Johannes A1 Weber, Manuela A1 Karl, Thomas A1 Breitenbach-Koller, Hannelore A1 Mülleder, Michael A1 Vowinckel, Jakob A1 Marx, Hans A1 Sauer, Michael A1 Mattanovich, Diethard A1 Ata, Özge A1 De, Sonakshi A1 Greslehner, Gregor P. A1 Geltinger, Florian A1 Burhans, Bill A1 Grant, Chris A1 Doronina, Victoria A1 Ralser, Meryem A1 Streubel, Maria Karolin A1 Grabner, Christian A1 Jarolim, Stefanie A1 Moßhammer, Claudia A1 Gourlay, Campbell W. A1 Hasek, Jiri A1 Cullen, Paul J. A1 Liti, Gianni A1 Ralser, Markus A1 Breitenbach, Michael YR 2020 UL http://www.g3journal.org/content/10/12/4637.abstract AB 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.