Evidence map›Paper›PMID 23341780›Full record

ArticlePLoS genetics2013

Multiple opposing constraints govern chromosome interactions during meiosis.

Doris Y Lui, Cori K Cahoon, Sean M Burgess

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Modeling homologous chromosome recognition via nonspecific interactions.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Article
  3. Diffusion and distal linkages govern interchromosomal dynamics during meiotic prophase.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Synaptonemal complex extension from clustered telomeres mediates full-length chromosome pairing in Schmidtea mediterranea.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  10. Article
  11. Review
  12. Article
  13. Article
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

3 authors at 1 institution in 1 country.

Doris Y LuiDepartment of Molecular and Cellular Biology, University of California Davis, Davis, California, United States of America.
Cori K Cahoon
Sean M Burgess
University of California, Davis · US

Funding

ENVIRONMENTAL TOXICOLOGYT32ES007059 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura S Van Winkle · 1985 to 2026
$7.9M
Homologous Chromosome Pairing in MeiosisR01GM075119 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BURGESS, SEAN M · 2006 to 2020
$4.8M
NIEHS NIH HHS NIH T32 ES07059NIEHS NIH HHS T32 ES007059NIGMS NIH HHS R01 GM075119NIGMS NIH HHS R01-GM075119
6 · The paper itself

Abstract

Homolog pairing and crossing over during meiosis I prophase is required for accurate chromosome segregation to form euploid gametes. The repair of Spo11-induced double-strand breaks (DSB) using a homologous chromosome template is a major driver of pairing in many species, including fungi, plants, and mammals. Inappropriate pairing and crossing over at ectopic loci can lead to chromosome rearrangements and aneuploidy. How (or if) inappropriate ectopic interactions are disrupted in favor of allelic interactions is not clear. Here we used an in vivo "collision" assay in budding yeast to test the contributions of cohesion and the organization and motion of chromosomes in the nucleus on promoting or antagonizing interactions between allelic and ectopic loci at interstitial chromosome sites. We found that deletion of the cohesin subunit Rec8, but not other chromosome axis proteins (e.g. Red1, Hop1, or Mek1), caused an increase in homolog-nonspecific chromosome interaction, even in the absence of Spo11. This effect was partially suppressed by expression of the mitotic cohesin paralog Scc1/Mdc1, implicating Rec8's role in cohesion rather than axis integrity in preventing nonspecific chromosome interactions. Disruption of telomere-led motion by treating cells with the actin polymerization inhibitor Latrunculin B (Lat B) elevated nonspecific collisions in rec8Δ spo11Δ. Next, using a visual homolog-pairing assay, we found that the delay in homolog pairing in mutants defective for telomere-led chromosome motion (ndj1Δ or csm4Δ) is enhanced in Lat B-treated cells, implicating actin in more than one process promoting homolog juxtaposition. We suggest that multiple, independent contributions of actin, cohesin, and telomere function are integrated to promote stable homolog-specific interactions and to destabilize weak nonspecific interactions by modulating the elastic spring-like properties of chromosomes.

Indexed as

EndodeoxyribonucleasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCell Cycle ProteinsCell NucleusChromosomal Proteins, Non-HistoneChromosome PairingChromosome SegregationCohesinsDNA Breaks, Double-StrandedMeiosisMeiotic Prophase IMeiotic Recombination Protein SPO11TelomereCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsEndodeoxyribonucleasesMCD1 protein, S cerevisiaeMeiotic Recombination Protein SPO11Saccharomyces cerevisiae ProteinsSpo11 protein, S cerevisiae

Identifiers

PMID23341780
PMCPMC3547833
OpenAlexW1968227580

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.