Evidence map›Paper›PMID 23902647›Full record

ArticleOpen biology2013

Positive regulation of meiotic DNA double-strand break formation by activation of the DNA damage checkpoint kinase Mec1(ATR).

Stephen Gray, Rachal M Allison, Valerie Garcia, Alastair S H Goldman, Matthew J Neale

Open access · goldAbstract read
In one paragraph

Article in Open biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
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  9. Review
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  11. Review
  12. Mechanism and Control of Meiotic DNA Double-Strand Break Formation inFrontiers in cell and developmental biology · 2021
    Review
  13. Phospho-Regulation of Meiotic Prophase.Frontiers in cell and developmental biology · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Dynamic recognition and repair of DNA complex damage.Journal of cellular physiology · 2019
    Article
  18. Review
  19. Article
  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

5 authors at 2 institutions in 1 country.

Stephen GrayMRC Genome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton BN1 9RQ, UK.
Rachal M Allison
Valerie Garcia
Alastair S H Goldman
Matthew J Neale
University of Sussex · GBUniversity of Sheffield · GB

Funding

Biotechnology and Biological Sciences Research Council G20296Medical Research Council G0800005
6 · The paper itself

Abstract

During meiosis, formation and repair of programmed DNA double-strand breaks (DSBs) create genetic exchange between homologous chromosomes-a process that is critical for reductional meiotic chromosome segregation and the production of genetically diverse sexually reproducing populations. Meiotic DSB formation is a complex process, requiring numerous proteins, of which Spo11 is the evolutionarily conserved catalytic subunit. Precisely how Spo11 and its accessory proteins function or are regulated is unclear. Here, we use Saccharomyces cerevisiae to reveal that meiotic DSB formation is modulated by the Mec1(ATR) branch of the DNA damage signalling cascade, promoting DSB formation when Spo11-mediated catalysis is compromised. Activation of the positive feedback pathway correlates with the formation of single-stranded DNA (ssDNA) recombination intermediates and activation of the downstream kinase, Mek1. We show that the requirement for checkpoint activation can be rescued by prolonging meiotic prophase by deleting the NDT80 transcription factor, and that even transient prophase arrest caused by Ndt80 depletion is sufficient to restore meiotic spore viability in checkpoint mutants. Our observations are unexpected given recent reports that the complementary kinase pathway Tel1(ATM) acts to inhibit DSB formation. We propose that such antagonistic regulation of DSB formation by Mec1 and Tel1 creates a regulatory mechanism, where the absolute frequency of DSBs is maintained at a level optimal for genetic exchange and efficient chromosome segregation.

Indexed as

DNA Breaks, Double-StrandedMeiosisCell Cycle ProteinsChromosome SegregationDNA-Binding ProteinsDNA RepairDNA, Single-StrandedEndodeoxyribonucleasesIntracellular Signaling Peptides and ProteinsMeiotic Recombination Protein SPO11MutationNuclear ProteinsProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscription FactorsCDC5 protein, S cerevisiaeCell Cycle ProteinsDNA-Binding ProteinsDNA, Single-StrandedEndodeoxyribonucleasesIntracellular Signaling Peptides and ProteinsMEC1 protein, S cerevisiaeMeiotic Recombination Protein SPO11NDT80 protein, S cerevisiaeNuclear ProteinsProtein Serine-Threonine KinasesRAD17 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSpo11 protein, S cerevisiaeTEL1 protein, S cerevisiaeTranscription FactorscheckpointMec1 ATRmeiosisrecombinationSpo11Tel1 ATM

Identifiers

PMID23902647
PMCPMC3728922
OpenAlexW2148713677

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.