Evidence map›Paper›PMID 22549958›Full record

ArticleGenes & development2012

Meiotic DNA double-strand breaks and chromosome asynapsis in mice are monitored by distinct HORMAD2-independent and -dependent mechanisms.

Lukasz Wojtasz, Jeffrey M Cloutier, Marek Baumann, Katrin Daniel, János Varga, Jun Fu, Konstantinos Anastassiadis, A Francis Stewart, Attila Reményi, James M A Turner and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing 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

103 citing papers in PubMed, 161 citations in OpenAlex.

  1. Article
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  4. Structure and function of the synaptonemal complex.The Journal of cell biology · 2026
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  14. BRCA1 safeguards genome integrity by activating chromosome asynapsis checkpoint to eliminate recombination-defective oocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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43 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 3 countries.

Lukasz WojtaszInstitute of Physiological Chemistry, Technische Universität Dresden, Dresden 01307, Germany.
Jeffrey M Cloutier
Marek Baumann
Katrin Daniel
János Varga
Jun Fu
Konstantinos Anastassiadis
A Francis Stewart
Attila Reményi
James M A Turner
Attila Tóth
TU Dresden · DEEötvös Loránd University · HUMedical Research Council · GB

Funding

Medical Research CouncilWellcome Trust 081665/Z/06/Z
6 · The paper itself

Abstract

Meiotic crossover formation involves the repair of programmed DNA double-strand breaks (DSBs) and synaptonemal complex (SC) formation. Completion of these processes must precede the meiotic divisions in order to avoid chromosome abnormalities in gametes. Enduring key questions in meiosis have been how meiotic progression and crossover formation are coordinated, whether inappropriate asynapsis is monitored, and whether asynapsis elicits prophase arrest via mechanisms that are distinct from the surveillance of unrepaired DNA DSBs. We disrupted the meiosis-specific mouse HORMAD2 (Hop1, Rev7, and Mad2 domain 2) protein, which preferentially associates with unsynapsed chromosome axes. We show that HORMAD2 is required for the accumulation of the checkpoint kinase ATR along unsynapsed axes, but not at DNA DSBs or on DNA DSB-associated chromatin loops. Consistent with the hypothesis that ATR activity on chromatin plays important roles in the quality control of meiotic prophase, HORMAD2 is required for the elimination of the asynaptic Spo11(-/-), but not the asynaptic and DSB repair-defective Dmc1(-/-) oocytes. Our observations strongly suggest that HORMAD2-dependent recruitment of ATR to unsynapsed chromosome axes constitutes a mechanism for the surveillance of asynapsis. Thus, we provide convincing evidence for the existence of a distinct asynapsis surveillance mechanism that safeguards the ploidy of the mammalian germline.

Indexed as

DNA Breaks, Double-StrandedAnimalsCell Cycle ProteinsChromosome PairingFemaleInfertility, MaleMaleMeiosisMiceMice, Mutant StrainsNuclear ProteinsOocytesPhosphate-Binding ProteinsSynaptonemal ComplexCell Cycle ProteinsDmc1 protein, mouseHORMAD2 protein, mouseNuclear ProteinsPhosphate-Binding Proteins

Identifiers

PMID22549958
PMCPMC3347793
OpenAlexW2140159026

What OpenQuestion holds

Textmetadata
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.