ArticlePloS one2014
Mechanistic study on the nuclear modifier gene MSS1 mutation suppressing neomycin sensitivity of the mitochondrial 15S rRNA C1477G mutation in Saccharomyces cerevisiae.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Neddylation inhibition induces glutamine uptake and metabolism by targeting CRL3Nature communications · 2022Article
- Neddylation regulation of mitochondrial structure and functions.Cell & bioscience · 2021Review
- LncRNAs regulate metabolism in cancer.International journal of biological sciences · 2020Review
- Inhibiting neddylation modification alters mitochondrial morphology and reprograms energy metabolism in cancer cells.JCI insight · 2019Article
- Identifying novel protein phenotype annotations by hybridizing protein-protein interactions and protein sequence similarities.Molecular genetics and genomics : MGG · 2016Article
- MTO1 worked as a modifier in the aminoglycosides sensitivity of yeast carrying a mitochondrial 15S rRNA C1477G mutation.PloS one · 2015Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phenotypic manifestation of mitochondrial DNA (mtDNA) mutations can be modulated by nuclear genes and environmental factors. However, neither the interaction among these factors nor their underlying mechanisms are well understood. The yeast Saccharomyces cerevisiae mtDNA 15S rRNA C1477G mutation (PR) corresponds to the human 12S rRNA A1555G mutation. Here we report that a nuclear modifier gene mss1 mutation suppresses the neomycin-sensitivity phenotype of a yeast C1477G mutant in fermentable YPD medium. Functional assays show that the mitochondrial function of the yeast C1477G mutant was impaired severely in YPD medium with neomycin. Moreover, the mss1 mutation led to a significant increase in the steady-state level of HAP5 (heme activated protein), which greatly up-regulated the expression of glycolytic transcription factors RAP1, GCR1, and GCR2 and thus stimulated glycolysis. Furthermore, the high expression of the key glycolytic enzyme genes HXK2, PFK1 and PYK1 indicated that enhanced glycolysis not only compensated for the ATP reduction from oxidative phosphorylation (OXPHOS) in mitochondria, but also ensured the growth of the mss1(PR) mutant in YPD medium with neomycin. This study advances our understanding of the phenotypic manifestation of mtDNA mutations.
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