ArticleCell cycle (Georgetown, Tex.)2012
Multiple phosphorylation of Rad9 by CDK is required for DNA damage checkpoint activation.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- From cell cycle control to cancer therapy: exploring the role of CDK1 and CDK2 in tumorigenesis.Medical oncology (Northwood, London, England) · 2025Review
- γH2A/γH2AX Mediates DNA Damage-Specific Control of Checkpoint Signaling inInternational journal of molecular sciences · 2024Article
- Yeast UPS1 deficiency leads to UVC radiation sensitivity and shortened lifespan.Antonie van Leeuwenhoek · 2023Article
- The budding yeast protein Chl1p is required for delaying progression through G1/S phase after DNA damage.Cell division · 2021Article
- A novel role for Dun1 in the regulation of origin firing upon hyper-acetylation of H3K56.PLoS genetics · 2021Article
- Pseudohyphal Growth of the Emerging Pathogen Candida auris Is Triggered by Genotoxic Stress through the S Phase Checkpoint.mSphere · 2020Article
- Investigation of the Possible Role of RAD9 in Post-Diapaused Embryonic Development of the Brine ShrimpGenes · 2019Article
- A cell cycle-independent mode of the Rad9-Dpb11 interaction is induced by DNA damage.Scientific reports · 2017Article
- TOPBP1The Journal of cell biology · 2017Article
- Non-canonical functions of cell cycle cyclins and cyclin-dependent kinases.Nature reviews. Molecular cell biology · 2016Review
- Enrichment of Cdk1-cyclins at DNA double-strand breaks stimulates Fun30 phosphorylation and DNA end resection.Nucleic acids research · 2016Article
- Knockdown of Rad9A enhanced DNA damage induced by trichostatin A in esophageal cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Yeast as a model system to study metabolic impact of selenium compounds.Microbial cell (Graz, Austria) · 2015Review
- Switch on the engine: how the eukaryotic replicative helicase MCM2-7 becomes activated.Chromosoma · 2015Review
- To trim or not to trim: progression and control of DSB end resection.Cell cycle (Georgetown, Tex.) · 2013Article
- The many roads to checkpoint activation.Cell cycle (Georgetown, Tex.) · 2012Article
- Preserving Yeast Genetic Heritage through DNA Damage Checkpoint Regulation and Telomere Maintenance.Biomolecules · 2012Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The DNA damage checkpoint controls cell cycle arrest in response to DNA damage, and activation of this checkpoint is in turn cell cycle-regulated. Rad9, the ortholog of mammalian 53BP1, is essential for this checkpoint response and is phosphorylated by the cyclin-dependent kinase (CDK) in the yeast Saccharomyces cerevisiae. Previous studies suggested that the CDK consensus sites of Rad9 are important for its checkpoint activity. However, the precise CDK sites of Rad9 involved have not been determined. Here we show that CDK consensus sites of Rad9 function in parallel to its BRCT domain toward checkpoint activation, analogous to its fission yeast ortholog Crb2. Unlike Crb2, however, mutation of multiple rather than any individual CDK site of Rad9 is required to completely eliminate its checkpoint activity in vivo. Although Dpb11 interacts with CDK-phosphorylated Rad9, we provide evidence showing that elimination of this interaction does not affect DNA damage checkpoint activation in vivo, suggesting that additional pathway(s) exist. Taken together, these findings suggest that the regulation of Rad9 by CDK and the role of Dpb11 in DNA damage checkpoint activation are more complex than previously suggested. We propose that multiple phosphorylation of Rad9 by CDK may provide a more robust system to allow Rad9 to control cell cycle-dependent DNA damage checkpoint activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.