Evidence map›Paper›PMID 26225562›Full record

ArticlePloS one2015

Essential and Checkpoint Functions of Budding Yeast ATM and ATR during Meiotic Prophase Are Facilitated by Differential Phosphorylation of a Meiotic Adaptor Protein, Hop1.

Ana Penedos, Anthony L Johnson, Emily Strong, Alastair S Goldman, Jesús A Carballo, Rita S Cha

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  12. Phospho-Regulation of Meiotic Prophase.Frontiers in cell and developmental biology · 2021
    Review
  13. Review
  14. Intragenic meiotic recombination in Schizosaccharomyces pombe is sensitive to environmental temperature changes.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2020
    Article
  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Ana PenedosDivision of Stem Cell Biology and Developmental Genetics, MRC National Institute for Medical Research, London, NW7 1AA, United Kingdom.
Anthony L JohnsonDivision of Stem Cell Biology and Developmental Genetics, MRC National Institute for Medical Research, London, NW7 1AA, United Kingdom.
Emily StrongDepartment of Molecular Biology and Biotechnology, The University of Sheffield, Sheffield, S10 2TN, United Kingdom.
Alastair S GoldmanDepartment of Molecular Biology and Biotechnology, The University of Sheffield, Sheffield, S10 2TN, United Kingdom.
Jesús A CarballoGenome Damage & Stability Centre, University of Sussex, Brighton, BN1 9RQ, United Kingdom.
Rita S ChaNorth West Cancer Research Fund Institute, School of Medical Sciences, Bangor University, Bangor, LL57 2UW, United Kingdom.
University of Sheffield · GBBangor University · GBUniversity of Sussex · GB

Funding

Medical Research Council G0801130Medical Research Council U1175.01.005.00005.01
6 · The paper itself

Abstract

A hallmark of the conserved ATM/ATR signalling is its ability to mediate a wide range of functions utilizing only a limited number of adaptors and effector kinases. During meiosis, Tel1 and Mec1, the budding yeast ATM and ATR, respectively, rely on a meiotic adaptor protein Hop1, a 53BP1/Rad9 functional analog, and its associated kinase Mek1, a CHK2/Rad53-paralog, to mediate multiple functions: control of the formation and repair of programmed meiotic DNA double strand breaks, enforcement of inter-homolog bias, regulation of meiotic progression, and implementation of checkpoint responses. Here, we present evidence that the multi-functionality of the Tel1/Mec1-to-Hop1/Mek1 signalling depends on stepwise activation of Mek1 that is mediated by Tel1/Mec1 phosphorylation of two specific residues within Hop1: phosphorylation at the threonine 318 (T318) ensures the transient basal level Mek1 activation required for viable spore formation during unperturbed meiosis. Phosphorylation at the serine 298 (S298) promotes stable Hop1-Mek1 interaction on chromosomes following the initial phospho-T318 mediated Mek1 recruitment. In the absence of Dmc1, the phospho-S298 also promotes Mek1 hyper-activation necessary for implementing meiotic checkpoint arrest. Taking these observations together, we propose that the Hop1 phospho-T318 and phospho-S298 constitute key components of the Tel1/Mec1- based meiotic recombination surveillance (MRS) network and facilitate effective coupling of meiotic recombination and progression during both unperturbed and challenged meiosis.

Indexed as

MeiosisDNA-Binding ProteinsDNA RepairPhosphorylationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSerineTemperatureDNA-Binding ProteinsHOP1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSerine

Identifiers

PMID26225562
PMCPMC4520594
OpenAlexW1784785746

What OpenQuestion holds

Textmetadata
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.