ArticleMolecular and cellular biology2004
Association of Rad9 with double-strand breaks through a Mec1-dependent mechanism.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- TPI and GAPDH Interact with Rad9, Linking Glycolytic Enzymes to Cancer.International journal of molecular sciences · 2026Article
- Yeast Nat4 regulates DNA damage checkpoint signaling through its N-terminal acetyltransferase activity on histone H4.PLoS genetics · 2024Article
- Rad9/53BP1 promotes DNA repair via crossover recombination by limiting the Sgs1 and Mph1 helicases.Nature communications · 2020Article
- Functional interplay between the oxidative stress response and DNA damage checkpoint signaling for genome maintenance in aerobic organisms.Journal of microbiology (Seoul, Korea) · 2020Review
- DNA damage kinase signaling: checkpoint and repair at 30 years.The EMBO journal · 2019Review
- Sae2 antagonizes Rad9 accumulation at DNA double-strand breaks to attenuate checkpoint signaling and facilitate end resection.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Sae2 Function at DNA Double-Strand Breaks Is Bypassed by Dampening Tel1 or Rad53 Activity.PLoS genetics · 2015Article
- The 9-1-1 checkpoint clamp coordinates resection at DNA double strand breaks.Nucleic acids research · 2015Article
- Yeast as a model system to study metabolic impact of selenium compounds.Microbial cell (Graz, Austria) · 2015Review
- Leveraging DNA damage response signaling to identify yeast genes controlling genome stability.G3 (Bethesda, Md.) · 2015Article
- Mec1/ATR regulates the generation of single-stranded DNA that attenuates Tel1/ATM signaling at DNA ends.The EMBO journal · 2014Article
- Ddc2 mediates Mec1 activation through a Ddc1- or Dpb11-independent mechanism.PLoS genetics · 2014Article
- Article
- Unligated Okazaki Fragments Induce PCNA Ubiquitination and a Requirement for Rad59-Dependent Replication Fork Progression.PloS one · 2013Article
- Activation of protein kinase Tel1 through recognition of protein-bound DNA ends.Molecular and cellular biology · 2011Article
- PhosphoGRID: a database of experimentally verified in vivo protein phosphorylation sites from the budding yeast Saccharomyces cerevisiae.Database : the journal of biological databases and curation · 2010Article
- Dissection of Rad9 BRCT domain function in the mitotic checkpoint response to telomere uncapping.DNA repair · 2009Article
- Rapid Cdc13 turnover and telomere length homeostasis are controlled by Cdk1-mediated phosphorylation of Cdc13.Nucleic acids research · 2009Article
- Maintenance of the DNA-damage checkpoint requires DNA-damage-induced mediator protein oligomerization.Molecular cell · 2009Article
- Activation of the budding yeast securin Pds1 but not Rad53 correlates with double-strand break-associated G2/M cell cycle arrest in a mec1 hypomorphic mutant.Cell cycle (Georgetown, Tex.) · 2007Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rad9 is required for the activation of DNA damage checkpoint pathways in budding yeast. Rad9 is phosphorylated after DNA damage in a Mec1- and Tel1-dependent manner and subsequently interacts with Rad53. This Rad9-Rad53 interaction has been suggested to trigger the activation and phosphorylation of Rad53. Here we show that Mec1 controls the Rad9 accumulation at double-strand breaks (DSBs). Rad9 was phosphorylated after DSB induction and associated with DSBs. However, its phosphorylation and association with DSBs were significantly decreased in cells carrying a mec1Delta or kinase-negative mec1 mutation. Mec1 phosphorylated the S/TQ motifs of Rad9 in vitro, the same motifs that are phosphorylated after DNA damage in vivo. In addition, multiple mutations in the Rad9 S/TQ motifs resulted in its defective association with DSBs. Phosphorylation of Rad9 was partially defective in cells carrying a weak mec1 allele (mec1-81), whereas its association with DSBs occurred efficiently in the mec1-81 mutants, as found in wild-type cells. However, the Rad9-Rad53 interaction after DSB induction was significantly decreased in mec1-81 mutants, as it was in mec1Delta mutants. Deletion mutation in RAD53 did not affect the association of Rad9 with DSBs. Our results suggest that Mec1 promotes association of Rad9 with sites of DNA damage, thereby leading to full phosphorylation of Rad9 and its interaction with Rad53.
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