ArticleFrontiers in cell and developmental biology2021
Mrc1-Dependent Chromatin Compaction Represses DNA Double-Stranded Break Repair by Homologous Recombination Upon Replication Stress.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 7 citations in OpenAlex.
- Replication Fork-Associated Checkpoint Mediator Mrc1/Claspin Acts in Arrest-Independent Double-Strand Break Survival.bioRxiv : the preprint server for biology · 2026Article
- Compound Library Screening Identified Cladribine as a Novel Radiosensitizer for Prostate Cancer.Cancer science · 2026Article
- Inhibition of DEK restores hematopoietic stem cell function in Fanconi anemia.The Journal of experimental medicine · 2025Article
- Effect and mechanism of signal peptide and maltose on recombinant type III collagen production in Pichia pastoris.Applied microbiology and biotechnology · 2023Article
- Genetic requirements for repair of lesions caused by single genomic ribonucleotides in S phase.Nature communications · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
The coordination of DNA replication and repair is critical for the maintenance of genome stability. It has been shown that the Mrc1-mediated S phase checkpoint inhibits DNA double-stranded break (DSB) repair through homologous recombination (HR). How the replication checkpoint inhibits HR remains only partially understood. Here we show that replication stress induces the suppression of both Sgs1/Dna2- and Exo1-mediated resection pathways in an Mrc1-dependent manner. As a result, the loading of the single-stranded DNA binding factor replication protein A (RPA) and Rad51 and DSB repair by HR were severely impaired under replication stress. Notably, the deletion of
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