ArticleScientific reports2017
A cell cycle-independent mode of the Rad9-Dpb11 interaction is induced by DNA damage.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Slx4 and Fun30/SMARCAD1 coordinate S-phase checkpoint regulation and replication fork protection in response to Top1-DNA crosslinks.Nucleic acids research · 2026Article
- DNA Damage and Replication Stress Checkpoints.Annual review of biochemistry · 2025Review
- γH2A/γH2AX Mediates DNA Damage-Specific Control of Checkpoint Signaling inInternational journal of molecular sciences · 2024Article
- The budding yeast protein Chl1p is required for delaying progression through G1/S phase after DNA damage.Cell division · 2021Article
- Rad9, a 53BP1 Ortholog of Budding Yeast, Is Insensitive to Spo11-Induced Double-Strand Breaks During Meiosis.Frontiers in cell and developmental biology · 2021Article
- Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020Review
- The Yeast PCNA Unloader Elg1 RFC-Like Complex Plays a Role in Eliciting the DNA Damage Checkpoint.mBio · 2019Article
- Article
- DDR Inc., one business, two associates.Current genetics · 2019Review
- Quantitative sensing and signalling of single-stranded DNA during the DNA damage response.Nature communications · 2019Article
- The Multifaceted Role of Rad9 in the DNA Damage Response of Saccharomyces cerevisiae.Yeast (Chichester, England)Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Budding yeast Rad9, like its orthologs, controls two aspects of the cellular response to DNA double strand breaks (DSBs) - signalling of the DNA damage checkpoint and DNA end resection. Rad9 binds to damaged chromatin via modified nucleosomes independently of the cell cycle phase. Additionally, Rad9 engages in a cell cycle-regulated interaction with Dpb11 and the 9-1-1 clamp, generating a second pathway that recruits Rad9 to DNA damage sites. Binding to Dpb11 depends on specific S/TP phosphorylation sites of Rad9, which are modified by cyclin-dependent kinase (CDK). Here, we show that these sites additionally become phosphorylated upon DNA damage. We define the requirements for DNA damage-induced S/TP phosphorylation of Rad9 and show that it is independent of the cell cycle or CDK activity but requires prior recruitment of Rad9 to damaged chromatin, indicating that it is catalysed by a chromatin-bound kinase. The checkpoint kinases Mec1 and Tel1 are required for Rad9 S/TP phosphorylation, but their influence is likely indirect and involves phosphorylation of Rad9 at S/TQ sites. Notably, DNA damage-induced S/TP phosphorylation triggers Dpb11 binding to Rad9, but the DNA damage-induced Rad9-Dpb11 interaction is dispensable for recruitment to DNA damage sites, indicating that the Rad9-Dpb11 interaction functions beyond Rad9 recruitment.
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