Evidence map›Paper›PMID 20150277›Full record

ArticleDevelopment (Cambridge, England)2010

The Trithorax group protein Ash2l and Saf-A are recruited to the inactive X chromosome at the onset of stable X inactivation.

Dieter Pullirsch, Renate Härtel, Hiroyuki Kishimoto, Martin Leeb, Günter Steiner, Anton Wutz

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 1% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Gene regulation in time and space during X-chromosome inactivation.Nature reviews. Molecular cell biology · 2022
    Review
  10. Article
  11. Review
  12. Genetics research · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. The B-side ofF1000Research · 2020
    Review
  17. Article
  18. Review
  19. Review
  20. Review

3 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

6 authors at 2 institutions in 2 countries.

Dieter PullirschResearch Institute of Molecular Pathology, Dr Bohr-Gasse 7, 1030 Vienna, Austria.
Renate Härtel
Hiroyuki Kishimoto
Martin Leeb
Günter Steiner
Anton Wutz
Research Institute of Molecular Pathology · ATMedical University of Vienna · AT

Funding

Medical Research Council G0800784Wellcome Trust 087530Wellcome Trust 087530/Z/08/A
6 · The paper itself

Abstract

Mammals compensate X chromosome gene dosage between the sexes by silencing of one of the two female X chromosomes. X inactivation is initiated in the early embryo and requires the non-coding Xist RNA, which encompasses the inactive X chromosome (Xi) and triggers its silencing. In differentiated cells, several factors including the histone variant macroH2A and the scaffold attachment factor SAF-A are recruited to the Xi and maintain its repression. Consequently, in female somatic cells the Xi remains stably silenced independently of Xist. Here, we identify the Trithorax group protein Ash2l as a novel component of the Xi. Ash2l is recruited by Xist concomitantly with Saf-A and macroH2A at the transition to Xi maintenance. Recruitment of these factors characterizes a developmental transition point for the chromatin composition of the Xi. Surprisingly, expression of a mutant Xist RNA that does not cause gene repression can trigger recruitment of Ash2l, Saf-A and macroH2A to the X chromosome, and can cause chromosome-wide histone H4 hypoacetylation. This suggests that a chromatin configuration is established on non-genic chromatin on the Xi by Xist to provide a repressive compartment that could be used for maintaining gene silencing. Gene silencing is mechanistically separable from the formation of this repressive compartment and, thus, requires additional pathways. This observation highlights a crucial role for spatial organization of chromatin changes in the maintenance of X inactivation.

Indexed as

3T3 CellsAnimalsCells, CulturedChromosomes, Human, XDNA-Binding ProteinsFemaleGene SilencingHeterochromatinHeterogeneous-Nuclear Ribonucleoprotein UHistonesHumansMiceNuclear ProteinsProtein BindingRNA, Long NoncodingRNA, UntranslatedASH2L protein, humanDNA-Binding ProteinsHeterochromatinHeterogeneous-Nuclear Ribonucleoprotein UHistonesmacroH2A histoneNuclear ProteinsRNA, Long NoncodingRNA, UntranslatedTranscription FactorsXIST non-coding RNA

Identifiers

PMID20150277
PMCPMC2834461
OpenAlexW2140847047

What OpenQuestion holds

Textmetadata
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.