Slow Growth and Increased Spontaneous Mutation Frequency in Respiratory Deficient afo1(-) Yeast Suppressed by a Dominant Mutation in ATP3

0537624 - MBÚ 2021 RIV US eng J - Journal Article
Li, J. - Rinnerthaler, M. - Hartl, J. - Weber, M. - Karl, T. - Breitenbach-Koller, H. - Mulleder, M. - Vowinckel, J. - Marx, H. - Sauer, M. - Mattanovich, D. - Ata, O. - De, S. - Greslehner, G. P. - Geltinger, F. - Burhans, B. - Grant, C. - Doronina, V. - Ralser, M. - Streubel, M. K. - Grabner, C. - Jarolim, S. - Mosshammer, C. - Gourlay, C. W. - Gourlay, C.W. - Hašek, Jiří - Cullen, P. J. - Liti, G. - Ralser, M. - Breitenbach, M.
Slow Growth and Increased Spontaneous Mutation Frequency in Respiratory Deficient afo1(-) Yeast Suppressed by a Dominant Mutation in ATP3.
G3-Genes, Genomes, Genetics. Roč. 10, č. 12 (2020), s. 4637-4648. ISSN 2160-1836. E-ISSN 2160-1836
Institutional support: RVO:61388971
Keywords : Saccharomyces cerevisiae * rho-zero * growth velocity * mutation frequency * atp3
OECD category: Microbiology
Impact factor: 3.154, year: 2020
Method of publishing: Open access
https://academic.oup.com/g3journal/article/10/12/4637/6048714?login=true

A yeast deletion mutation in the nuclear-encoded gene, 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 (-) 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 gene. Comparing isogenic slowly growing rho-zero and rapidly growing suppressed (-) 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 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.
Permanent Link: http://hdl.handle.net/11104/0315437