ArticleNucleic acids research2015
Two separable functions of Ctp1 in the early steps of meiotic DNA double-strand break repair.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Insight into meiotic DNA end resection: Mechanisms and regulation.DNA repair · 2025Review
- A conserved Ctp1/CtIP C-terminal peptide stimulates Mre11 endonuclease activity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Distributing meiotic crossovers for optimal fertility and evolution.DNA repair · 2019Review
- CDK contribution to DSB formation and recombination in fission yeast meiosis.PLoS genetics · 2019Article
- Article
- Rev7 and 53BP1/Crb2 prevent RecQ helicase-dependent hyper-resection of DNA double-strand breaks.eLife · 2018Article
- Genetic Separation of Sae2 Nuclease Activity from Mre11 Nuclease Functions in Budding Yeast.Molecular and cellular biology · 2017Article
- CtIP/Ctp1/Sae2, molecular form fit for function.DNA repair · 2017Review
- Ctp1-dependent clipping and resection of DNA double-strand breaks by Mre11 endonuclease complex are not genetically separable.Nucleic acids research · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Meiotic programmed DNA double-strand break (DSB) repair is essential for crossing-over and viable gamete formation and requires removal of Spo11-oligonucleotide complexes from 5' ends (clipping) and their resection to generate invasive 3'-end single-stranded DNA (resection). Ctp1 (Com1, Sae2, CtIP homolog) acting with the Mre11-Rad50-Nbs1 (MRN) complex is required in both steps. We isolated multiple S. pombe ctp1 mutants deficient in clipping but proficient in resection during meiosis. Remarkably, all of the mutations clustered in or near the conserved CxxC or RHR motif in the C-terminal portion. The mutants tested, like ctp1Δ, were clipping-deficient by both genetic and physical assays-. But, unlike ctp1Δ, these mutants were recombination-proficient for Rec12 (Spo11 homolog)-independent break-repair and resection-proficient by physical assay. We conclude that the intracellular Ctp1 C-terminal portion is essential for clipping, while the N-terminal portion is sufficient for DSB end-resection. This conclusion agrees with purified human CtIP resection and endonuclease activities being independent. Our mutants provide intracellular evidence for separable functions of Ctp1. Some mutations truncate Ctp1 in the same region as one of the CtIP mutations linked to the Seckel and Jawad severe developmental syndromes, suggesting that these syndromes are caused by a lack of clipping at DSB ends that require repair.
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