ArticleThe Journal of cell biology2009
Oncogene homologue Sch9 promotes age-dependent mutations by a superoxide and Rev1/Polzeta-dependent mechanism.
Article in The Journal of cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 72 citations in OpenAlex.
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- Adaptation to Fasting in Crucian Carp (Carassius auratus): Gut Microbiota and Its Correlative Relationship with Immune Function.Microbial ecology · 2019Article
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- Overproduction of Sch9 leads to its aggregation and cell elongation in Saccharomyces cerevisiae.PloS one · 2018Article
- Protective effects of short-term dietary restriction in surgical stress and chemotherapy.Ageing research reviews · 2017Review
- Regenerative Medicine: Shedding Light on the Link between Aging and Cancer.Cell transplantation · 2017Review
- Metabolic Alterations at the Crossroad of Aging and Oncogenesis.International review of cell and molecular biology · 2017Review
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- High reactive oxygen species levels are detected at the end of the chronological life span of translocant yeast cells.Molecular genetics and genomics : MGG · 2016Article
- Starvation promotes REV1 SUMOylation and p53-dependent sensitization of melanoma and breast cancer cells.Cancer research · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Oncogenes contribute to tumorigenesis by promoting growth and inhibiting apoptosis. Here we examine the function of Sch9, the Saccharomyces cerevisiae homologue of the mammalian Akt and S6 kinase, in DNA damage and genomic instability during aging in nondividing cells. Attenuation of age-dependent increases in base substitutions, small DNA insertions/deletions, and gross chromosomal rearrangements (GCRs) in sch9Delta mutants is associated with increased mitochondrial superoxide dismutase (MnSOD) expression, decreased DNA oxidation, reduced REV1 expression and translesion synthesis, and elevated resistance to oxidative stress-induced mutagenesis. Deletion of REV1, the lack of components of the error-prone Polzeta, or the overexpression of SOD1 or SOD2 is sufficient to reduce age-dependent point mutations in SCH9 overexpressors, but REV1 deficiency causes a major increase in GCRs. These results suggest that the proto-oncogene homologue Sch9 promotes the accumulation of superoxide-dependent DNA damage in nondividing cells, which induces error-prone DNA repair that generates point mutations to avoid GCRs and cell death during the first round of replication.
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Registered trials
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