Evidence map›Paper›PMID 30383767›Full record

ArticlePLoS genetics2018

The tumor suppressor BRCA1-BARD1 complex localizes to the synaptonemal complex and regulates recombination under meiotic dysfunction in Caenorhabditis elegans.

Qianyan Li, Takamune T Saito, Marina Martinez-Garcia, Alison J Deshong, Saravanapriah Nadarajan, Katherine S Lawrence, Paula M Checchi, Monica P Colaiacovo, JoAnne Engebrecht

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
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

38 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. microPublication biology · 2024
    Article
  6. One of these strains is not like the others:microPublication biology · 2024
    Article
  7. Article
  8. Article
  9. Meiotic DNA exchanges inLife science alliance · 2023
    Article
  10. Article
  11. Cells · 2023
    Article
  12. Article
  13. microPublication biology · 2023
    Article
  14. Oogenesis in Caenorhabditis elegans.Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. Loss of NSE-4 Perturbs Genome Stability and DNA Repair inInternational journal of molecular sciences · 2022
    Article
  19. Article
  20. Review
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

9 authors at 2 institutions in 1 country.

Qianyan LiDepartment of Molecular and Cellular Biology, University of California Davis; Davis CA, United States of America.
Takamune T SaitoDepartment of Genetics, Harvard Medical School; Boston, MA, United States of America.
Marina Martinez-GarciaDepartment of Genetics, Harvard Medical School; Boston, MA, United States of America.ORCID 0000-0001-8491-2557
Alison J DeshongDepartment of Molecular and Cellular Biology, University of California Davis; Davis CA, United States of America.
Saravanapriah NadarajanDepartment of Genetics, Harvard Medical School; Boston, MA, United States of America.ORCID 0000-0001-5273-4514
Katherine S LawrenceDepartment of Molecular and Cellular Biology, University of California Davis; Davis CA, United States of America.
Paula M ChecchiDepartment of Molecular and Cellular Biology, University of California Davis; Davis CA, United States of America.
Monica P ColaiacovoDepartment of Genetics, Harvard Medical School; Boston, MA, United States of America.ORCID 0000-0001-7803-4372
JoAnne EngebrechtDepartment of Molecular and Cellular Biology, University of California Davis; Davis CA, United States of America.ORCID 0000-0002-2733-7506
University of California, Davis · USHarvard University · US

Funding

UC Davis MCB T32 Administrative Supplement to Recognize Excellence in Diversity, Equity, Inclusion, and Accessibility (DEIA) MentorshipT32GM007377 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI CHEDIN, FREDERIC LOUIS · 1985 to 2023
$9.9M
Synaptonemal Complex Assembly and Function in MeiosisR01GM072551 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI Monica P Colaiacovo · 2005 to 2026
$7.5M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
Training Program in Oncogenic Signals and Chromosome BiologyT32CA108459 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HEYER, WOLF-DIETRICH · 2006 to 2020
$3.6M
Sex-specific regulation of meiosisR01GM103860 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ENGEBRECHT, JOANNE · 2013 to 2021
$2.4M
Molecular mechanisms of germline DNA repair and DNA damage responseR01GM105853 · NIGMS · HARVARD MEDICAL SCHOOL · PI COLAIACOVO, MONICA P · 2014 to 2017
$1.3M
NCI NIH HHS T32 CA108459NIGMS NIH HHS R01 GM072551NIGMS NIH HHS R01 GM103860NIGMS NIH HHS R01 GM105853NIGMS NIH HHS T32 GM007377NIH HHS P40 OD010440
6 · The paper itself

Abstract

Breast cancer susceptibility gene 1 (BRCA1) and binding partner BRCA1-associated RING domain protein 1 (BARD1) form an essential E3 ubiquitin ligase important for DNA damage repair and homologous recombination. The Caenorhabditis elegans orthologs, BRC-1 and BRD-1, also function in DNA damage repair, homologous recombination, as well as in meiosis. Using functional GFP fusions we show that in mitotically-dividing germ cells BRC-1 and BRD-1 are nucleoplasmic with enrichment at foci that partially overlap with the recombinase RAD-51. Co-localization with RAD-51 is enhanced under replication stress. As cells enter meiosis, BRC-1-BRD-1 remains nucleoplasmic and in foci, and beginning in mid-pachytene the complex co-localizes with the synaptonemal complex. Following establishment of the single asymmetrically positioned crossover on each chromosome pair, BRC-1-BRD-1 concentrates to the short arm of the bivalent. Localization dependencies reveal that BRC-1 and BRD-1 are interdependent and the complex fails to properly localize in both meiotic recombination and chromosome synapsis mutants. Consistent with a role for BRC-1-BRD-1 in meiotic recombination in the context of the synaptonemal complex, inactivation of BRC-1 or BRD-1 enhances the embryonic lethality of mutants defective in chromosome synapsis. Our data suggest that under meiotic dysfunction, BRC-1-BRD-1 stabilizes the RAD-51 filament and alters the recombination landscape; these two functions can be genetically separated from BRC-1-BRD-1's role in the DNA damage response. Together, we propose that BRC-1-BRD-1 serves a checkpoint function at the synaptonemal complex where it monitors and modulates meiotic recombination.

Indexed as

Recombination, GeneticAllelesAnimalsBRCA1 ProteinCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA ReplicationEmbryo, NonmammalianGenes, ReporterGerm CellsMeiosisProtein TransportRad51 RecombinaseRecombinant Fusion ProteinsSynaptonemal ComplexTumor Suppressor ProteinsBARD1 protein, humanBRCA1 ProteinBRCA1 protein, humanCaenorhabditis elegans Proteinsrad-51 protein, C elegansRad51 RecombinaseRecombinant Fusion ProteinsTumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID30383767
PMCPMC6211623
OpenAlexW2953141930

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.