%0 Journal Article
%T Slow Growth and Increased Spontaneous Mutation Frequency in Respiratory Deficient afo1- Yeast Suppressed by a Dominant Mutation in ATP3.
%A Li J
%A Rinnerthaler M
%A Hartl J
%A Weber M
%A Karl T
%A Breitenbach-Koller H
%A Mülleder M
%A Vowinckel J
%A Marx H
%A Sauer M
%A Mattanovich D
%A Ata Ö
%A De S
%A Greslehner GP
%A Geltinger F
%A Burhans B
%A Grant C
%A Doronina V
%A Ralser M
%A Streubel MK
%A Grabner C
%A Jarolim S
%A Moßhammer C
%A Gourlay CW
%A Hasek J
%A Cullen PJ
%A Liti G
%A Ralser M
%A Breitenbach M
%J G3 (Bethesda)
%V 10
%N 12
%D 12 2020 3
%M 33093184
%F 3.542
%R 10.1534/g3.120.401537
%X 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.