Evidence map›Paper›PMID 23555294›Full record

ArticlePLoS genetics2013

Mouse HFM1/Mer3 is required for crossover formation and complete synapsis of homologous chromosomes during meiosis.

Michel F Guiraldelli, Craig Eyster, Joseph L Wilkerson, Michael E Dresser, Roberto J Pezza

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 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

71 citing papers in PubMed, 118 citations in OpenAlex.

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  13. HEIP1 orchestrates pro-crossover protein activity during mammalian meiosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  19. Article
  20. Genetic insights into the complexity of premature ovarian insufficiency.Reproductive biology and endocrinology : RB&E · 2024
    Review

11 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

5 authors at 2 institutions in 1 country.

Michel F GuiraldelliOklahoma Medical Research Foundation, Oklahoma City, Oklahoma, United States of America.
Craig Eyster
Joseph L Wilkerson
Michael E Dresser
Roberto J Pezza
Oklahoma Medical Research Foundation · USUniversity of Oklahoma Health Sciences Center · US

Funding

Mechanics and regulation of chromosome dynamics in meiotic prophaseR01GM087516 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI DRESSER, MICHAEL EDWARD · 2009 to 2012
$1.5M
NIGMS NIH HHS R01 GM087516
6 · The paper itself

Abstract

Faithful chromosome segregation during meiosis requires that homologous chromosomes associate and recombine. Chiasmata, the cytological manifestation of recombination, provide the physical link that holds the homologs together as a pair, facilitating their orientation on the spindle at meiosis I. Formation of most crossover (CO) events requires the assistance of a group of proteins collectively known as ZMM. HFM1/Mer3 is in this group of proteins and is required for normal progression of homologous recombination and proper synapsis between homologous chromosomes in a number of model organisms. Our work is the first study in mammals showing the in vivo function of mouse HFM1. Cytological observations suggest that initial steps of recombination are largely normal in a majority of Hfm1(-/-) spermatocytes. Intermediate and late stages of recombination appear aberrant, as chromosomal localization of MSH4 is altered and formation of MLH1foci is drastically reduced. In agreement, chiasma formation is reduced, and cells arrest with subsequent apoptosis at diakinesis. Our results indicate that deletion of Hfm1 leads to the elimination of a major fraction but not all COs. Formation of chromosome axial elements and homologous pairing is apparently normal, and Hfm1(-/-) spermatocytes progress to the end of prophase I without apparent developmental delay or apoptosis. However, synapsis is altered with components of the central region of the synaptonemal complex frequently failing to extend the full length of the chromosome axes. We propose that initial steps of recombination are sufficient to support homology recognition, pairing, and initial chromosome synapsis and that HFM1 is required to form normal numbers of COs and to complete synapsis.

Indexed as

Crossing Over, GeneticSpermatocytesAnimalsApoptosisChromosome PairingChromosomesDNA HelicasesHumansMaleMeiosisMiceRecombination, GeneticDNA HelicasesHFM1 protein, humanHFM1 protein, mouse

Identifiers

PMID23555294
PMCPMC3605105
OpenAlexW1974717740

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LicenceCC BY
Read underepoch 390

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.