Evidence map›Paper›PMID 25053665›Full record

ArticleGenetics2014

DNA helicase HIM-6/BLM both promotes MutSγ-dependent crossovers and antagonizes MutSγ-independent interhomolog associations during caenorhabditis elegans meiosis.

Mara Schvarzstein, Divya Pattabiraman, Diana E Libuda, Ajit Ramadugu, Angela Tam, Enrique Martinez-Perez, Baptiste Roelens, Karl A Zawadzki, Rayka Yokoo, Simona Rosu and 4 more

Abstract read
In one paragraph

Article in Genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. High-resolution global recombination mapping inbioRxiv : the preprint server for biology · 2026
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Mara SchvarzsteinDepartments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, California 94305.
Divya PattabiramanDepartments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, California 94305.
Diana E LibudaDepartments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, California 94305.
Ajit RamaduguDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan 48109-2200.
Angela TamDepartments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, California 94305.
Enrique Martinez-PerezMRC Clinical Sciences Centre, Imperial College Faculty of Medicine, London, United Kingdom.
Baptiste RoelensDepartments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, California 94305.
Karl A ZawadzkiDepartments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, California 94305.
Rayka YokooDepartments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, California 94305.
Simona RosuDepartments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, California 94305.
Aaron F SeversonDepartment of Biology, Geology, Environmental Science, Cleveland State University, Cleveland, Ohio 44115.
Barbara J MeyerHoward Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, California 94720.
Kentaro NabeshimaDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan 48109-2200.
Anne M VilleneuveDepartments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, California 94305 annev@stanford.edu.

Funding

INSTITUTIONAL TRAINING GRANT IN GENOME SCIENCET32HG000044 · NHGRI · STANFORD UNIVERSITY · PI MICHAEL P. SNYDER · 1995 to 2026
$32.2M
GENETICS TRAINING PROGRAM FOR PHD CANDIDATEST32GM007790 · NIGMS · STANFORD UNIVERSITY · PI BRUNET, ANNE, KINGSLEY, DAVID M · 1985 to 2020
$12.8M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
MEIOTIC CHROMOSOME SEGREGATION IN C. ELEGANSR01GM053804 · NIGMS · STANFORD UNIVERSITY · PI VILLENEUVE, ANNE M · 1996 to 2017
$5.7M
Genetic Recombination of c. ElegansR01GM067268 · NIGMS · STANFORD UNIVERSITY · PI VILLENEUVE, ANNE M · 2003 to 2017
$4.6M
Recombination pathway and partner choice during C. elegans meiosisR00HD076165 · NICHD · UNIVERSITY OF OREGON · PI LIBUDA, DIANA ELIZABETH · 2015 to 2017
$719k
Recombination pathway and partner choice during C. elegans meiosisK99HD076165 · NICHD · STANFORD UNIVERSITY · PI LIBUDA, DIANA ELIZABETH · 2013 to 2014
$196k
CIHRHoward Hughes Medical InstituteMedical Research Council MC_U120097113NHGRI NIH HHS T32 HG000044NICHD NIH HHS K99 HD076165NICHD NIH HHS R00 HD076165NIGMS NIH HHS R01 GM053804NIGMS NIH HHS R01 GM067268NIGMS NIH HHS R01GM53804NIGMS NIH HHS R01GM67268NIGMS NIH HHS T32 GM007790NIH HHS P40 OD010440
6 · The paper itself

Abstract

Meiotic recombination is initiated by the programmed induction of double-strand DNA breaks (DSBs), lesions that pose a potential threat to the genome. A subset of the DSBs induced during meiotic prophase become designated to be repaired by a pathway that specifically yields interhomolog crossovers (COs), which mature into chiasmata that temporarily connect the homologs to ensure their proper segregation at meiosis I. The remaining DSBs must be repaired by other mechanisms to restore genomic integrity prior to the meiotic divisions. Here we show that HIM-6, the Caenorhabditis elegans ortholog of the RecQ family DNA helicase BLM, functions in both of these processes. We show that him-6 mutants are competent to load the MutSγ complex at multiple potential CO sites, to generate intermediates that fulfill the requirements of monitoring mechanisms that enable meiotic progression, and to accomplish and robustly regulate CO designation. However, recombination events at a subset of CO-designated sites fail to mature into COs and chiasmata, indicating a pro-CO role for HIM-6/BLM that manifests itself late in the CO pathway. Moreover, we find that in addition to promoting COs, HIM-6 plays a role in eliminating and/or preventing the formation of persistent MutSγ-independent associations between homologous chromosomes. We propose that HIM-6/BLM enforces biased outcomes of recombination events to ensure that both (a) CO-designated recombination intermediates are reliably resolved as COs and (b) other recombination intermediates reliably mature into noncrossovers in a timely manner.

Indexed as

Crossing Over, GeneticAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA-Binding ProteinsMeiosisCaenorhabditis elegans ProteinsDNA-Binding ProteinsHIM-6 protein, C elegansMSH-5 protein, C elegansBLM helicaseCaenorhabditis elegansmeiosisMutSγrecombination

Identifiers

PMID25053665
PMCPMC4174932

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.