<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(1)</volume><submitter>di Cicco G</submitter><pubmed_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</pubmed_abstract><journal>Scientific reports</journal><pagination>11650</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5599684</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A cell cycle-independent mode of the Rad9-Dpb11 interaction is induced by DNA damage.</pubmed_title><pmcid>PMC5599684</pmcid><pubmed_authors>di Cicco G</pubmed_authors><pubmed_authors>Bantele SCS</pubmed_authors><pubmed_authors>Reusswig KU</pubmed_authors><pubmed_authors>Pfander B</pubmed_authors></additional><is_claimable>false</is_claimable><name>A cell cycle-independent mode of the Rad9-Dpb11 interaction is induced by DNA damage.</name><description>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</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Sep</publication><modification>2025-04-05T14:17:45.441Z</modification><creation>2019-03-27T02:56:27Z</creation></dates><accession>S-EPMC5599684</accession><cross_references><pubmed>28912563</pubmed><doi>10.1038/s41598-017-11937-z</doi></cross_references></HashMap>