Evidence map›Paper›PMID 27462424›Full record

ArticleCell discovery2015

Senataxin controls meiotic silencing through ATR activation and chromatin remodeling.

Abrey J Yeo, Olivier J Becherel, John E Luff, Mark E Graham, Derek Richard, Martin F Lavin

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
–field-weighted citation impact, top 88% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 0 citations in OpenAlex.

  1. Pooled it
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  9. Review
  10. Article
  11. Sex body: A nest of protein mixture.Frontiers in cell and developmental biology · 2023
    Review
  12. Review
  13. Article
  14. Integrated genome and transcriptome analyses reveal the mechanism of genome instability in ataxia with oculomotor apraxia 2.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Review
  16. Review
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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 1 institution in 1 country.

Abrey J YeoThe University of Queensland, UQ Centre for Clinical Research (UQCCR), Brisbane, QLD, Australia; School of Medicine, The University of Queensland, Herston, Brisbane, QLD, Australia.
Olivier J BecherelThe University of Queensland, UQ Centre for Clinical Research (UQCCR), Brisbane, QLD, Australia; School of Chemistry and Molecular Biosciences, The University of Queensland, St Lucia, Brisbane, QLD, Australia.
John E LuffThe University of Queensland, UQ Centre for Clinical Research (UQCCR) , Brisbane, QLD, Australia.
Mark E GrahamChildren's Medical Research Institute, The University of Sydney , Westmead, NSW, Australia.
Derek RichardCancer and Ageing Research Program, Faculty of Health, Queensland University of Technology , Brisbane, QLD, Australia.
Martin F LavinThe University of Queensland, UQ Centre for Clinical Research (UQCCR), Brisbane, QLD, Australia; School of Medicine, The University of Queensland, Herston, Brisbane, QLD, Australia.
University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senataxin, defective in ataxia oculomotor apraxia type 2, protects the genome by facilitating the resolution of RNA-DNA hybrids (R-loops) and other aspects of RNA processing. Disruption of this gene in mice causes failure of meiotic recombination and defective meiotic sex chromosome inactivation, leading to male infertility. Here we provide evidence that the disruption of Setx leads to reduced SUMOylation and disruption of protein localization across the XY body during meiosis. We demonstrate that senataxin and other DNA damage repair proteins, including ataxia telangiectasia and Rad3-related protein-interacting partner, are SUMOylated, and a marked downregulation of both ataxia telangiectasia and Rad3-related protein-interacting partner and TopBP1 leading to defective activation and signaling through ataxia telangiectasia and Rad3-related protein occurs in the absence of senataxin. Furthermore, chromodomain helicase DNA-binding protein 4, a component of the nucleosome remodeling and deacetylase chromatin remodeler that interacts with both ataxia telangiectasia and Rad3-related protein and senataxin was not recruited efficiently to the XY body, triggering altered histone acetylation and chromatin conformation in Setx (-/-) pachytene-staged spermatocytes. These results demonstrate that senataxin has a critical role in ataxia telangiectasia and Rad3-related protein- and chromodomain helicase DNA-binding protein 4-mediated transcriptional silencing and chromatin remodeling during meiosis providing greater insight into its critical role in gene regulation to protect against neurodegeneration.

Indexed as

chromatin remodelingDNA damage repairmeiosissenataxintranscription

Identifiers

PMID27462424
PMCPMC4860845
OpenAlexW2337287858

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.