Evidence map›Paper›PMID 27257060›Full record

ArticleNucleic acids research2016

The Pch2 AAA+ ATPase promotes phosphorylation of the Hop1 meiotic checkpoint adaptor in response to synaptonemal complex defects.

Esther Herruzo, David Ontoso, Sara González-Arranz, Santiago Cavero, Ana Lechuga, Pedro A San-Segundo

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 49 citations in OpenAlex.

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  13. SCFLife science alliance · 2021
    Article
  14. Phospho-Regulation of Meiotic Prophase.Frontiers in cell and developmental biology · 2021
    Review
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  16. Article
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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

6 authors at 3 institutions in 1 country.

Esther HerruzoInstituto de Biología Funcional y Genómica. Consejo Superior de Investigaciones Científicas and University of Salamanca, 37007 Salamanca, Spain.
David OntosoInstituto de Biología Funcional y Genómica. Consejo Superior de Investigaciones Científicas and University of Salamanca, 37007 Salamanca, Spain.
Sara González-ArranzInstituto de Biología Funcional y Genómica. Consejo Superior de Investigaciones Científicas and University of Salamanca, 37007 Salamanca, Spain.
Santiago CaveroInstituto de Biología Funcional y Genómica. Consejo Superior de Investigaciones Científicas and University of Salamanca, 37007 Salamanca, Spain.
Ana LechugaInstituto de Biología Funcional y Genómica. Consejo Superior de Investigaciones Científicas and University of Salamanca, 37007 Salamanca, Spain.
Pedro A San-SegundoInstituto de Biología Funcional y Genómica. Consejo Superior de Investigaciones Científicas and University of Salamanca, 37007 Salamanca, Spain pedross@usal.es.
Consejo Superior de Investigaciones Científicas · ESInstituto de Biología Funcional y Genómica · ESUniversidad de Salamanca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Meiotic cells possess surveillance mechanisms that monitor critical events such as recombination and chromosome synapsis. Meiotic defects resulting from the absence of the synaptonemal complex component Zip1 activate a meiosis-specific checkpoint network resulting in delayed or arrested meiotic progression. Pch2 is an evolutionarily conserved AAA+ ATPase required for the checkpoint-induced meiotic block in the zip1 mutant, where Pch2 is only detectable at the ribosomal DNA array (nucleolus). We describe here that high levels of the Hop1 protein, a checkpoint adaptor that localizes to chromosome axes, suppress the checkpoint defect of a zip1 pch2 mutant restoring Mek1 activity and meiotic cell cycle delay. We demonstrate that the critical role of Pch2 in this synapsis checkpoint is to sustain Mec1-dependent phosphorylation of Hop1 at threonine 318. We also show that the ATPase activity of Pch2 is essential for its checkpoint function and that ATP binding to Pch2 is required for its localization. Previous work has shown that Pch2 negatively regulates Hop1 chromosome abundance during unchallenged meiosis. Based on our results, we propose that, under checkpoint-inducing conditions, Pch2 also possesses a positive action on Hop1 promoting its phosphorylation and its proper distribution on unsynapsed chromosome axes.

Indexed as

Cell Cycle CheckpointsMeiosisAdenosine TriphosphatasesAdenosine TriphosphateBinding SitesChromosome PairingDNA-Binding ProteinsDNA Breaks, Double-StrandedGenes, SuppressorGenetic TestingMicrobial ViabilityModels, BiologicalMutationNuclear ProteinsPhosphoprotein PhosphatasesPhosphorylationAdenosine TriphosphatasesAdenosine TriphosphateDNA-Binding ProteinsHOP1 protein, S cerevisiaeNuclear ProteinsPch2 protein, S cerevisiaePhosphoprotein PhosphatasesSaccharomyces cerevisiae Proteins

Identifiers

PMID27257060
PMCPMC5027488
OpenAlexW2416802580

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.