ArticleeLife2016
MutSα maintains the mismatch repair capability by inhibiting PCNA unloading.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Human PMS1-dependent non-canonical mismatch repair engages with MBD4 to repair methylated CpG deamination.Nucleic acids research · 2026Article
- DNA mismatch repair mediated by Mlh1-Pms1 endonuclease-catalyzed mispair excision.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mlh1-Pms1 couples ATP-driven DNA compaction with nick-dependent endonuclease activation.Nucleic acids research · 2025Article
- Mlh1-Pms1 ATPase activity is regulated distinctly by self-generated nicks and strand discrimination signals in mismatch repair.Nucleic acids research · 2025Article
- Crossover recombination between homologous chromosomes in meiosis: recent progress and remaining mysteries.Trends in genetics : TIG · 2025Review
- Preparation of Nucleoplasmic Extract and Its Application in DNA End Processing.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Action-At-A-Distance in DNA Mismatch Repair: Mechanistic Insights and Models for How DNA and Repair Proteins Facilitate Long-Range Communication.Biomolecules · 2024Review
- The Mlh1-Pms1 endonuclease uses ATP to preserve DNA discontinuities as strand discrimination signals to facilitate mismatch repair.bioRxiv : the preprint server for biology · 2024Article
- Resection of DNA double-strand breaks activates Mre11-Rad50-Nbs1- and Rad9-Hus1-Rad1-dependent mechanisms that redundantly promote ATR checkpoint activation and end processing in Xenopus egg extracts.Nucleic acids research · 2024Article
- The Atad5 RFC-like complex is the major unloader of proliferating cell nuclear antigen in Xenopus egg extracts.The Journal of biological chemistry · 2024Article
- Multi-omic analysis in normal colon organoids highlights MSH4 as a novel marker of defective mismatch repair in Lynch syndrome and microsatellite instability.Cancer medicine · 2023Article
- The mismatch repair endonuclease MutLα tethers duplex regions of DNA together and relieves DNA torsional tension.Nucleic acids research · 2023Article
- Anti-recombination function of MutSα restricts telomere extension by ALT-associated homology-directed repair.Cell reports · 2021Article
- DNA Repair in Haploid Context.International journal of molecular sciences · 2021Review
- Handcuffing intrinsically disordered regions in Mlh1-Pms1 disrupts mismatch repair.Nucleic acids research · 2021Article
- Strand discrimination in DNA mismatch repair.DNA repair · 2021Review
- Article
- Experimental exchange of paralogous domains in the MLH family provides evidence of sub-functionalization after gene duplication.G3 (Bethesda, Md.) · 2021Article
- Review
- Ligation of newly replicated DNA controls the timing of DNA mismatch repair.Current biology : CB · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eukaryotic mismatch repair (MMR) utilizes single-strand breaks as signals to target the strand to be repaired. DNA-bound PCNA is also presumed to direct MMR. The MMR capability must be limited to a post-replicative temporal window during which the signals are available. However, both identity of the signal(s) involved in the retention of this temporal window and the mechanism that maintains the MMR capability after DNA synthesis remain unclear. Using Xenopus egg extracts, we discovered a mechanism that ensures long-term retention of the MMR capability. We show that DNA-bound PCNA induces strand-specific MMR in the absence of strand discontinuities. Strikingly, MutSα inhibited PCNA unloading through its PCNA-interacting motif, thereby extending significantly the temporal window permissive to strand-specific MMR. Our data identify DNA-bound PCNA as the signal that enables strand discrimination after the disappearance of strand discontinuities, and uncover a novel role of MutSα in the retention of the post-replicative MMR capability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.