ArticleNucleic acids research2016
Dual daughter strand incision is processive and increases the efficiency of DNA mismatch repair.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Redundant mispair excision mechanisms in eukaryotic DNA mismatch repair.Nucleus (Austin, Tex.) · 2026Review
- A complete DNA repair system assembled by two endosymbionts restores heat tolerance of the insect host.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Real-time monitoring of replication errors' fate reveals the origin and dynamics of spontaneous mutations.Nature communications · 2024Article
- The mismatch repair endonuclease MutLα tethers duplex regions of DNA together and relieves DNA torsional tension.Nucleic acids research · 2023Article
- Pan-cancer analyses reveal IGSF10 as an immunological and prognostic biomarker.Frontiers in genetics · 2022Article
- Handcuffing intrinsically disordered regions in Mlh1-Pms1 disrupts mismatch repair.Nucleic acids research · 2021Article
- Strand discrimination in DNA mismatch repair.DNA repair · 2021Review
- The selection process of licensing a DNA mismatch for repair.Nature structural & molecular biology · 2021Article
- The unstructured linker arms of MutL enable GATC site incision beyond roadblocks during initiation of DNA mismatch repair.Nucleic acids research · 2019Article
- MutL sliding clamps coordinate exonuclease-independent Escherichia coli mismatch repair.Nature communications · 2019Article
- Intrinsically disordered regions regulate both catalytic and non-catalytic activities of the MutLα mismatch repair complex.Nucleic acids research · 2019Article
- Stochastic Processes and Component Plasticity Governing DNA Mismatch Repair.Journal of molecular biology · 2018Review
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA mismatch repair (MMR) is an evolutionarily-conserved process responsible for the repair of replication errors. In Escherichia coli, MMR is initiated by MutS and MutL, which activate MutH to incise transiently-hemimethylated GATC sites. MMR efficiency depends on the distribution of these GATC sites. To understand which molecular events determine repair efficiency, we quantitatively studied the effect of strand incision on unwinding and excision activity. The distance between mismatch and GATC site did not influence the strand incision rate, and an increase in the number of sites enhanced incision only to a minor extent. Two GATC sites were incised by the same activated MMR complex in a processive manner, with MutS, the closed form of MutL and MutH displaying different roles. Unwinding and strand excision were more efficient on a substrate with two nicks flanking the mismatch, as compared to substrates containing a single nick or two nicks on the same side of the mismatch. Introduction of multiple nicks by the human MutLα endonuclease also contributed to increased repair efficiency. Our data support a general model of prokaryotic and eukaryotic MMR in which, despite mechanistic differences, mismatch-activated complexes facilitate efficient repair by creating multiple daughter strand nicks.
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