ArticleeLife2017
Concerted action of the MutLβ heterodimer and Mer3 helicase regulates the global extent of meiotic gene conversion.
Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 81 citations in OpenAlex.
- Pharmacologic Inhibition of PMS2 Induces MMR Deficiency and Response to Immune Checkpoint Blockade.Cancer discovery · 2026Article
- Crossover formation and coordinated assembly of synaptonemal complex relies on a direct interaction between Zip1 and Zip3.Genetics · 2026Article
- RPA directly stimulates Mer3 helicase processivity to ensure normal crossover formation in meiosis.Nature communications · 2026Article
- Mismatch repair MLH complexes make distinct contributions to post-replicative mismatch repair versus trinucleotide repeat expansions.bioRxiv : the preprint server for biology · 2026Article
- The GHKL ATPase Family as a Paradigm for MutL Homolog Function in DNA Mismatch Repair.International journal of molecular sciences · 2025Review
- Crossover formation and coordinated assembly of synaptonemal complex relies on a direct interaction between Zip1 and Zip3.bioRxiv : the preprint server for biology · 2025Article
- Rad51, Rad54, and ZMM proteins antagonize the mismatch repair system to promote fertility of budding yeast intraspecies hybrid zygotes.Nucleic acids research · 2025Article
- MutLγ enforces meiotic crossovers in Arabidopsis thaliana.Nucleic acids research · 2025Article
- In vivo CRISPR-Cas9 genome editing in mice identifies genetic modifiers of somatic CAG repeat instability in Huntington's disease.Nature genetics · 2025Article
- Proximity labeling reveals new functional relationships between meiotic recombination proteins in S. cerevisiae.PLoS genetics · 2024Article
- HLTF disrupts Cas9-DNA post-cleavage complexes to allow DNA break processing.Nature communications · 2024Article
- The Dmc1 recombinase physically interacts with and promotes the meiotic crossover functions of the Mlh1-Mlh3 endonuclease.Genetics · 2024Article
- The molecular machinery of meiotic recombination.Biochemical Society transactions · 2024Review
- The Dmc1 recombinase physically interacts with and promotes the meiotic crossover functions of the Mlh1-Mlh3 endonuclease.bioRxiv : the preprint server for biology · 2023Article
- Biochemical characterisation of Mer3 helicase interactions and the protection of meiotic recombination intermediates.Nucleic acids research · 2023Article
- The mismatch repair endonuclease MutLα tethers duplex regions of DNA together and relieves DNA torsional tension.Nucleic acids research · 2023Article
- WRN helicase and mismatch repair complexes independently and synergistically disrupt cruciform DNA structures.The EMBO journal · 2023Article
- The effect of DNA polymorphisms and natural variation on crossover hotspot activity in Arabidopsis hybrids.Nature communications · 2023Article
- Lessons from the meiotic recombination landscape of the ZMM deficient budding yeast Lachancea waltii.PLoS genetics · 2023Article
- Loss of Heterozygosity Spectrum Depends on Ploidy Level in Natural Yeast Populations.Molecular biology and evolution · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gene conversions resulting from meiotic recombination are critical in shaping genome diversification and evolution. How the extent of gene conversions is regulated is unknown. Here we show that the budding yeast mismatch repair related MutLβ complex, Mlh1-Mlh2, specifically interacts with the conserved meiotic Mer3 helicase, which recruits it to recombination hotspots, independently of mismatch recognition. This recruitment is essential to limit gene conversion tract lengths genome-wide, without affecting crossover formation. Contrary to expectations, Mer3 helicase activity, proposed to extend the displacement loop (D-loop) recombination intermediate, does not influence the length of gene conversion events, revealing non-catalytical roles of Mer3. In addition, both purified Mer3 and MutLβ preferentially recognize D-loops, providing a mechanism for limiting gene conversion in vivo. These findings show that MutLβ is an integral part of a new regulatory step of meiotic recombination, which has implications to prevent rapid allele fixation and hotspot erosion in populations.
Indexed as
Identifiers
What OpenQuestion holds
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.