Evidence map›Paper›PMID 23300481›Full record

ArticlePLoS genetics2013

MCM8 is required for a pathway of meiotic double-strand break repair independent of DMC1 in Arabidopsis thaliana.

Wayne Crismani, Virginie Portemer, Nicole Froger, Liudmila Chelysheva, Christine Horlow, Nathalie Vrielynck, Raphaël Mercier

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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Structural Activation of DNA Unwinding by MCM8/9/HROB.bioRxiv : the preprint server for biology · 2026
    Article
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  3. Frontiers in plant science · 2026
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  8. Review
  9. Article
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  11. Review
  12. Article
  13. Review
  14. ThePNAS nexus · 2023
    Article
  15. Crossover interference mechanism: New lessons from plants.Frontiers in cell and developmental biology · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

7 authors at 2 institutions in 1 country.

Wayne CrismaniINRA, UMR1318, Institut Jean-Pierre Bourgin, RD10, Versailles, France.
Virginie Portemer
Nicole Froger
Liudmila Chelysheva
Christine Horlow
Nathalie Vrielynck
Raphaël Mercier
AgroParisTech · FRInstitut Jean-Pierre Bourgin · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mini-chromosome maintenance (MCM) 2-9 proteins are related helicases. The first six, MCM2-7, are essential for DNA replication in all eukaryotes. In contrast, MCM8 is not always conserved in eukaryotes but is present in Arabidopsis thaliana. MCM8 is required for 95% of meiotic crossovers (COs) in Drosophila and is essential for meiosis completion in mouse, prompting us to study this gene in Arabidopsis meiosis. Three allelic Atmcm8 mutants showed a limited level of chromosome fragmentation at meiosis. This defect was dependent on programmed meiotic double-strand break (DSB) formation, revealing a role for AtMCM8 in meiotic DSB repair. In contrast, CO formation was not affected, as shown both genetically and cytologically. The Atmcm8 DSB repair defect was greatly amplified in the absence of the DMC1 recombinase or in mutants affected in DMC1 dynamics (sds, asy1). The Atmcm8 fragmentation defect was also amplified in plants heterozygous for a mutation in either recombinase, DMC1 or RAD51. Finally, in the context of absence of homologous chromosomes (i.e. haploid), mutation of AtMCM8 also provoked a low level of chromosome fragmentation. This fragmentation was amplified by the absence of DMC1 showing that both MCM8 and DMC1 can promote repair on the sister chromatid in Arabidopsis haploids. Altogether, this establishes a role for AtMCM8 in meiotic DSB repair, in parallel to DMC1. We propose that MCM8 is involved with RAD51 in a backup pathway that repairs meiotic DSB without giving CO when the major pathway, which relies on DMC1, fails.

Indexed as

Cell Cycle ProteinsRec A RecombinasesRecombination, GeneticArabidopsisArabidopsis ProteinsChromatidsCrossing Over, GeneticDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA HelicasesDNA RepairMeiosisMutationRad51 RecombinaseRecombinasesArabidopsis ProteinsATDMC1 protein, ArabidopsisATRAD51 protein, ArabidopsisCell Cycle ProteinsDNA-Binding ProteinsDNA HelicasesMCM8 protein, ArabidopsisRad51 RecombinaseRec A RecombinasesRecombinases

Identifiers

PMID23300481
PMCPMC3536722
OpenAlexW2047427992

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.