ArticleMolecular and cellular biology2004
The functions of budding yeast Sae2 in the DNA damage response require Mec1- and Tel1-dependent phosphorylation.
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 76 papers.
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Who cites it
76 citing papers in PubMed.
- Sae2 integrates CDK and checkpoint phosphorylation to coordinate MRX cleavage with checkpoint attenuation.Communications biology · 2025Article
- Insight into meiotic DNA end resection: Mechanisms and regulation.DNA repair · 2025Review
- Functional and molecular insights into the role of Sae2 C-terminus in the activation of MRX endonuclease.Nucleic acids research · 2024Article
- The Chromatin Landscape around DNA Double-Strand Breaks in Yeast and Its Influence on DNA Repair Pathway Choice.International journal of molecular sciences · 2023Review
- Sir3 heterochromatin protein promotes non-homologous end joining by direct inhibition of Sae2.The EMBO journal · 2022Article
- Phospho-Regulation of Meiotic Prophase.Frontiers in cell and developmental biology · 2021Review
- Mechanisms underlying genome instability mediated by formation of foldback inversions ineLife · 2020Article
- Hof1 plays a checkpoint-related role in MMS-induced DNA damage response inMolecular biology of the cell · 2020Article
- CDK and Mec1/Tel1-catalyzed phosphorylation of Sae2 regulate different responses to DNA damage.Nucleic acids research · 2019Article
- Activation of Tel1The Journal of biological chemistry · 2019Article
- Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context.Frontiers in molecular biosciences · 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
- Review
- Regulatory control of DNA end resection by Sae2 phosphorylation.Nature communications · 2018Article
- ATR is a multifunctional regulator of male mouse meiosis.Nature communications · 2018Article
- Processing of DNA Ends in the Maintenance of Genome Stability.Frontiers in genetics · 2018Review
- Article
- Chromatin stiffening underlies enhanced locus mobility after DNA damage in budding yeast.The EMBO journal · 2017Article
- Nucleolytic processing of aberrant replication intermediates by an Exo1-Dna2-Sae2 axis counteracts fork collapse-driven chromosome instability.Nucleic acids research · 2016Article
- Genetic and biochemical evidences reveal novel insights into the mechanism underlyingJournal of biosciences · 2016Article
16 more citing papers are in PubMed but not listed here.
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5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA damage checkpoint pathways sense DNA lesions and transduce the signals into appropriate biological responses, including cell cycle arrest, induction of transcriptional programs, and modification or activation of repair factors. Here we show that the Saccharomyces cerevisiae Sae2 protein, known to be involved in processing meiotic and mitotic double-strand breaks, is required for proper recovery from checkpoint-mediated cell cycle arrest after DNA damage and is phosphorylated periodically during the unperturbed cell cycle and in response to DNA damage. Both cell cycle- and DNA damage-dependent Sae2 phosphorylation requires the main checkpoint kinase, Mec1, and the upstream components of its pathway, Ddc1, Rad17, Rad24, and Mec3. Another pathway, involving Tel1 and the MRX complex, is also required for full DNA damage-induced Sae2 phosphorylation, that is instead independent of the downstream checkpoint transducers Rad53 and Chk1, as well as of their mediators Rad9 and Mrc1. Mutations altering all the favored ATM/ATR phosphorylation sites of Sae2 not only abolish its in vivo phosphorylation after DNA damage but also cause hypersensitivity to methyl methanesulfonate treatment, synthetic lethality with RAD27 deletion, and decreased rates of mitotic recombination between inverted Alu repeats, suggesting that checkpoint-mediated phosphorylation of Sae2 is important to support its repair and recombination functions.
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