ArticleMolecular and cellular biology2013
Deacetylase Rpd3 facilitates checkpoint adaptation by preventing Rad53 overactivation.
Article in Molecular and cellular biology, 2013. 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, 13 citations in OpenAlex.
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- Building a KATalogue of acetyllysine targeting and function.Briefings in functional genomics · 2016Review
- Cmr1/WDR76 defines a nuclear genotoxic stress body linking genome integrity and protein quality control.Nature communications · 2015Article
- Protein acetylation and acetyl coenzyme a metabolism in budding yeast.Eukaryotic cell · 2014Review
- Tos4 mediates gene expression homeostasis through interaction with HDAC complexes independently of H3K56 acetylation.The Journal of biological chemistryArticle
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DNA damage checkpoint is tightly controlled. After its activation, the checkpoint machinery is inactivated once lesions are repaired or undergoes adaptation if the DNA damage is unable to be repaired. Protein acetylation has been shown to play an important role in DNA damage checkpoint activation. However, the role of acetylation in checkpoint inactivation is unclear. Here we show that histone deacetylase Rpd3-mediated deacetylation of Rad53 plays an important role in checkpoint adaptation. Deletion of Rpd3 or inhibition of its activity impairs adaptation. RPD3 deletion also leads to a higher acetylation level and enhanced kinase activity of Rad53. Replacement of two major acetylation sites of Rad53 with arginine reduces its activity and further suppresses the adaptation defect of rpd3Δ cells, indicating that Rpd3 facilitates adaptation by preventing Rad53 overactivation. Similar to its role in adaptation, deletion of RPD3 or inhibition of its activity also suppressed checkpoint recovery. Altogether, our findings reveal an important role of Rpd3 in promoting checkpoint adaptation via deacetylation and inhibition of Rad53.
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