Evidence map›Paper›PMID 24385936›Full record

ArticlePLoS genetics2013

Smc5/6-Mms21 prevents and eliminates inappropriate recombination intermediates in meiosis.

Martin Xaver, Lingzhi Huang, Doris Chen, Franz Klein

Abstract 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 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing 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

53 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Multifaceted roles of SUMO in DNA metabolism.Nucleus (Austin, Tex.) · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. DNA segment capture by Smc5/6 holocomplexes.Nature structural & molecular biology · 2023
    Article
  11. Article
  12. Article
  13. Multiple Roles of SMC5/6 Complex during Plant Sexual Reproduction.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. Natural variation identifies SNI1, the SMC5/6 component, as a modifier of meiotic crossover inProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Article
  18. Article
  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

4 authors.

Martin XaverMax Perutz Laboratories, Chromosome Biology, University of Vienna, Vienna Biocenter, Vienna, Austria.
Lingzhi HuangMax Perutz Laboratories, Chromosome Biology, University of Vienna, Vienna Biocenter, Vienna, Austria.
Doris ChenMax Perutz Laboratories, Chromosome Biology, University of Vienna, Vienna Biocenter, Vienna, Austria.
Franz KleinMax Perutz Laboratories, Chromosome Biology, University of Vienna, Vienna Biocenter, Vienna, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Repairing broken chromosomes via joint molecule (JM) intermediates is hazardous and therefore strictly controlled in most organisms. Also in budding yeast meiosis, where production of enough crossovers via JMs is imperative, only a subset of DNA breaks are repaired via JMs, closely regulated by the ZMM pathway. The other breaks are repaired to non-crossovers, avoiding JM formation, through pathways that require the BLM/Sgs1 helicase. "Rogue" JMs that escape the ZMM pathway and BLM/Sgs1 are eliminated before metaphase by resolvases like Mus81-Mms4 to prevent chromosome nondisjunction. Here, we report the requirement of Smc5/6-Mms21 for antagonizing rogue JMs via two mechanisms; destabilizing early intermediates and resolving JMs. Elimination of the Mms21 SUMO E3-ligase domain leads to transient JM accumulation, depending on Mus81-Mms4 for resolution. Absence of Smc6 leads to persistent rogue JMs accumulation, preventing chromatin separation. We propose that the Smc5/6-Mms21 complex antagonizes toxic JMs by coordinating helicases and resolvases at D-Loops and HJs, respectively.

Indexed as

Cell Cycle ProteinsChromosome SegregationDNA Breaks, Double-StrandedDNA, CruciformDNA RepairHomologous RecombinationMeiosisMultiprotein ComplexesRecQ HelicasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSUMO-1 ProteinUbiquitin-Protein LigasesCell Cycle ProteinsDNA, CruciformMms21 protein, S cerevisiaeMultiprotein ComplexesRecQ HelicasesSaccharomyces cerevisiae ProteinsSGS1 protein, S cerevisiaeSMC5 protein, S cerevisiaeSUMO-1 ProteinUbiquitin-Protein Ligases

Identifiers

PMID24385936
PMCPMC3873250

What OpenQuestion holds

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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.