RT Journal Article
SR Electronic
T1 Slow Growth and Increased Spontaneous Mutation Frequency in Respiratory Deficient <em>afo1</em><sup>-</sup> Yeast Suppressed by a Dominant Mutation in <em>ATP3</em>
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.