ArticleScientific reports2018
Rpb9-deficient cells are defective in DNA damage response and require histone H3 acetylation for survival.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 12 citations in OpenAlex.
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- Purine Auxotrophic Starvation Evokes Phenotype Similar to Stationary Phase Cells in Budding Yeast.Journal of fungi (Basel, Switzerland) · 2021Article
- Comprehensive Bioinformatics Analysis IdentifiesFrontiers in genetics · 2021Article
- Taf14 is required for the stabilization of transcription pre-initiation complex in Saccharomyces cerevisiae.Epigenetics & chromatin · 2020Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
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Abstract
Rpb9 is a non-essential subunit of RNA polymerase II that is involved in DNA transcription and repair. In budding yeast, deletion of RPB9 causes several phenotypes such as slow growth and temperature sensitivity. We found that simultaneous mutation of multiple N-terminal lysines within histone H3 was lethal in rpb9Δ cells. Our results indicate that hypoacetylation of H3 leads to inefficient repair of DNA double-strand breaks, while activation of the DNA damage checkpoint regulators γH2A and Rad53 is suppressed in Rpb9-deficient cells. Combination of H3 hypoacetylation with the loss of Rpb9 leads to genomic instability, aberrant segregation of chromosomes in mitosis, and eventually to cell death. These results indicate that H3 acetylation becomes essential for efficient DNA repair and cell survival if a DNA damage checkpoint is defective.
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