ArticleThe Journal of biological chemistry2015
Phosphorylation of Sae2 Mediates Forkhead-associated (FHA) Domain-specific Interaction and Regulates Its DNA Repair Function.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- 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
- Ligand recognition by 14-3-3 proteins requires negative charges but not necessarily phosphorylation.FEBS letters · 2025Article
- Negative Charges, Not Necessary Phosphorylation, are Required for Ligand Recognition by 14-3-3 Proteins.bioRxiv : the preprint server for biology · 2024Article
- Sir3 heterochromatin protein promotes non-homologous end joining by direct inhibition of Sae2.The EMBO journal · 2022Article
- Mechanism and Control of Meiotic DNA Double-Strand Break Formation inFrontiers in cell and developmental biology · 2021Review
- DNA damage checkpoint and repair: From the budding yeastComputational and structural biotechnology journal · 2021Review
- CDK and Mec1/Tel1-catalyzed phosphorylation of Sae2 regulate different responses to DNA damage.Nucleic acids research · 2019Article
- DNA damage kinase signaling: checkpoint and repair at 30 years.The EMBO journal · 2019Review
- NBS1 promotes the endonuclease activity of the MRE11-RAD50 complex by sensing CtIP phosphorylation.The EMBO journal · 2019Article
- Article
- A Co-Expression Network in Hexaploid Wheat Reveals Mostly Balanced Expression and Lack of Significant Gene Loss of Homeologous Meiotic Genes Upon Polyploidization.Frontiers in plant science · 2019Article
- 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
- Xrs2 and Tel1 Independently Contribute to MR-Mediated DNA Tethering and Replisome Stability.Cell reports · 2018Article
- Enhancement of BLM-DNA2-Mediated Long-Range DNA End Resection by CtIP.Cell reports · 2017Article
- CtIP/Ctp1/Sae2, molecular form fit for function.DNA repair · 2017Review
- Genetic and biochemical evidences reveal novel insights into the mechanism underlyingJournal of biosciences · 2016Article
- Xrs2 Dependent and Independent Functions of the Mre11-Rad50 Complex.Molecular cell · 2016Article
- The MRX Complex Ensures NHEJ Fidelity through Multiple Pathways Including Xrs2-FHA-Dependent Tel1 Activation.PLoS genetics · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Saccharomyces cerevisiae Sae2 and its ortholog CtIP in higher eukaryotes have a conserved role in the initial processing of DNA lesions and influencing their subsequent repair pathways. Sae2 is phosphorylated by the ATR/ATM family kinases Mec1 and Tel1 in response to DNA damage. Among the Mec1/Tel1 consensus phosphorylation sites of Sae2, we found that mutations of Thr-90 and Thr-279 of Sae2 into alanine caused a persistent Rad53 activation in response to a transient DNA damage, similar to the loss of Sae2. To gain insight into the function of this phosphorylation of Sae2, we performed a quantitative proteomics analysis to identify its associated proteins. We found that phosphorylation of Thr-90 of Sae2 mediates its interaction with Rad53, Dun1, Xrs2, Dma1, and Dma2, whereas Rad53 and Dun1 additionally interact with phosphorylated Thr-279 of Sae2. Mutations of the ligand-binding residues of Forkhead-associated (FHA) domains of Rad53, Dun1, Xrs2, Dma1, and Dma2 abolished their interactions with Sae2, revealing the involvement of FHA-specific interactions. Mutations of Thr-90 and Thr-279 of Sae2 caused a synergistic defect when combined with sgs1Δ and exo1Δ and elevated gross chromosomal rearrangements. Likewise, mutations of RAD53 and DUN1 caused a synthetic growth defect with sgs1Δ and elevated gross chromosomal rearrangements. These findings suggest that threonine-specific phosphorylation of Sae2 by Mec1 and Tel1 contributes to DNA repair and genome maintenance via its interactions with Rad53 and Dun1.
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