Evidence map›Paper›PMID 25375142›Full record

ArticlePLoS genetics2014

The CSN/COP9 signalosome regulates synaptonemal complex assembly during meiotic prophase I of Caenorhabditis elegans.

Heather Brockway, Nathan Balukoff, Martha Dean, Benjamin Alleva, Sarit Smolikove

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Active maintenance of meiosis-specific chromosome structures inProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Active maintenance of meiosis-specific chromosome structures inbioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Article
  6. Make it or break it: Protein homeostasis in the synaptonemal complex.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Increasing the Unneddylated Cullin1 Portion Rescues theMolecular and cellular biology · 2017
    Article
  18. Meiosis.WormBook : the online review of C. elegans biology · 2017
    Review
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Heather BrockwayInterdisciplinary Program in Genetics, University of Iowa, Iowa City, Iowa, United States of America.
Nathan BalukoffDepartment of Biology, University of Iowa, Iowa City, Iowa, United States of America.
Martha DeanDepartment of Biology, University of Iowa, Iowa City, Iowa, United States of America.
Benjamin AllevaDepartment of Biology, University of Iowa, Iowa City, Iowa, United States of America.
Sarit SmolikoveInterdisciplinary Program in Genetics, University of Iowa, Iowa City, Iowa, United States of America; Department of Biology, University of Iowa, Iowa City, Iowa, United States of America.
University of Iowa · US

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM008629 · NIGMS · UNIVERSITY OF IOWA · PI EBERL, DANIEL F · 1997 to 2021
$4.1M
NIGMS NIH HHS T32 GM008629
6 · The paper itself

Abstract

The synaptonemal complex (SC) is a conserved protein structure that holds homologous chromosome pairs together throughout much of meiotic prophase I. It is essential for the formation of crossovers, which are required for the proper segregation of chromosomes into gametes. The assembly of the SC is likely to be regulated by post-translational modifications. The CSN/COP9 signalosome has been shown to act in many pathways, mainly via the ubiquitin degradation/proteasome pathway. Here we examine the role of the CSN/COP9 signalosome in SC assembly in the model organism C. elegans. Our work shows that mutants in three subunits of the CSN/COP9 signalosome fail to properly assemble the SC. In these mutants, SC proteins aggregate, leading to a decrease in proper pairing between homologous chromosomes. The reduction in homolog pairing also results in an accumulation of recombination intermediates and defects in repair of meiotic DSBs to form the designated crossovers. The effect of the CSN/COP9 signalosome mutants on synapsis and crossover formation is due to increased neddylation, as reducing neddylation in these mutants can partially suppress their phenotypes. We also find a marked increase in apoptosis in csn mutants that specifically eliminates nuclei with aggregated SC proteins. csn mutants exhibit defects in germline proliferation, and an almost complete pachytene arrest due to an inability to activate the MAPK pathway. The work described here supports a previously unknown role for the CSN/COP9 signalosome in chromosome behavior during meiotic prophase I.

Indexed as

Crossing Over, GeneticAnimalsCaenorhabditis elegansChromosome PairingChromosome SegregationCOP9 Signalosome ComplexDNA DamageDNA RepairMeiosisMeiotic Prophase IMitogen-Activated Protein Kinase KinasesMultiprotein ComplexesMutationPeptide HydrolasesSignal TransductionSynaptonemal ComplexCOP9 Signalosome ComplexMitogen-Activated Protein Kinase KinasesMultiprotein ComplexesPeptide Hydrolases

Identifiers

PMID25375142
PMCPMC4222726
OpenAlexW2054147201

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.