ArticleGenetics2009
Polymorphisms in multiple genes contribute to the spontaneous mitochondrial genome instability of Saccharomyces cerevisiae S288C strains.
Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.
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Who cites it
111 citing papers in PubMed, 208 citations in OpenAlex.
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- QTL mapping, breeding, and debugging Saccharomyces cerevisiae strains through Reiterated Mass Selection and backcrosSing (ReMaSSing).Biotechnology for biofuels and bioproducts · 2026Article
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- The yeast Mkt1/Pbp1 complex promotes adaptive responses to respiratory growth.The Journal of cell biology · 2025Article
- High-resolution, genotype-free mapping of genetic variation with CRI-SPA-Map.bioRxiv : the preprint server for biology · 2025Article
- rDNA copy number variation affects yeast fitness in response to different environments.Genetics · 2025Article
- Inheritance bias of deletion-harbouring mtDNA in yeast: The role of copy number and intracellular selection.PLoS genetics · 2025Article
- Spermidine toxicity in Saccharomyces cerevisiae due to mitochondrial complex III deficiency.Biogerontology · 2025Article
- Construction and iterative redesign of synXVI a 903 kb synthetic Saccharomyces cerevisiae chromosome.Nature communications · 2025Article
- Plasticity and environment-specific relationships between gene expression and fitness in Saccharomyces cerevisiae.Nature ecology & evolution · 2024Article
- Mitochondrial Genome Instability inBiology · 2024Article
- The Yeast Ribosomal Protein Rpl1b Is Not Required for Respiration.International journal of molecular sciences · 2024Article
- Spontaneous single-nucleotide substitutions and microsatellite mutations have distinct distributions of fitness effects.PLoS biology · 2024Article
- Loss of mitochondrial DNA is associated with reduced DNA content variability inmicroPublication biology · 2024Article
- Spontaneous Mutations inInternational journal of molecular sciences · 2023Article
51 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
The mitochondrial genome (mtDNA) is required for normal cellular function; inherited and somatic mutations in mtDNA lead to a variety of diseases. Saccharomyces cerevisiae has served as a model to study mtDNA integrity, in part because it can survive without mtDNA. A measure of defective mtDNA in S. cerevisiae is the formation of petite colonies. The frequency at which spontaneous petite colonies arise varies by approximately 100-fold between laboratory and natural isolate strains. To determine the genetic basis of this difference, we applied quantitative trait locus (QTL) mapping to two strains at the opposite extremes of the phenotypic spectrum: the widely studied laboratory strain S288C and the vineyard isolate RM11-1a. Four main genetic determinants explained the phenotypic difference. Alleles of SAL1, CAT5, and MIP1 contributed to the high petite frequency of S288C and its derivatives by increasing the formation of petite colonies. By contrast, the S288C allele of MKT1 reduced the formation of petite colonies and compromised the growth of petite cells. The former three alleles were found in the EM93 strain, the founder that contributed approximately 88% of the S288C genome. Nearly all of the phenotypic difference between S288C and RM11-1a was reconstituted by introducing the common alleles of these four genes into the S288C background. In addition to the nuclear gene contribution, the source of the mtDNA influenced its stability. These results demonstrate that a few rare genetic variants with individually small effects can have a profound phenotypic effect in combination. Moreover, the polymorphisms identified in this study open new lines of investigation into mtDNA maintenance.
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