Evidence map›Paper›PMID 16980619›Full record

ArticleMolecular and cellular biology2006

Hematopoietic precursor cells transiently reestablish permissiveness for X inactivation.

Fabio Savarese, Katja Flahndorfer, Rudolf Jaenisch, Meinrad Busslinger, Anton Wutz

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

72 citing papers in PubMed, 147 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Cdk8 and Hira mutations trigger X chromosome elimination in naive female hybrid mouse embryonic stem cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. The Influence of Sex Hormones and X Chromosome in Immune Responses.Current topics in microbiology and immunology · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. Article

12 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

5 authors at 3 institutions in 2 countries.

Fabio SavareseResearch Institute of Molecular Pathology, Vienna Biocenter, Dr. Bohr-Gasse 7, 1030 Vienna, Austria.
Katja Flahndorfer
Rudolf Jaenisch
Meinrad Busslinger
Anton Wutz
Vienna Biocenter · ATResearch Institute of Molecular Pathology · ATWhitehead Institute for Biomedical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Xist is the trigger for X inactivation in female mammals. The long noncoding Xist RNA localizes along one of the two female X chromosomes and initiates chromosome-wide silencing in the early embryo. In differentiated cells, Xist becomes dispensable for the maintenance of the inactive X, and its function for initiation of silencing is lost. How Xist mediates gene repression remains an open question. Here, we use an inducible Xist allele in adult mice to identify cells in which Xist can cause chromosome-wide silencing. We show that Xist has the ability to initiate silencing in immature hematopoietic precursor cells. In contrast, hematopoietic stem cells and mature blood cells are unable to initiate ectopic X inactivation. This indicates that pathways critical for silencing are transiently activated in hematopoietic differentiation. Xist-responsive cell types in normal female mice show a change of chromatin marks on the inactive X. However, dosage compensation is maintained throughout hematopoiesis. Therefore, Xist can initiate silencing in precursors with concomitant maintenance of dosage compensation. This suggests that Xist function is restricted in development by the limited activity of epigenetic pathways rather than by a change in the responsiveness of chromatin between embryonic and differentiated cell types.

Indexed as

AllelesAnemiaAnimalsBone Marrow CellsCell DifferentiationCells, CulturedEmbryo, MammalianFemaleFlow CytometryGene SilencingGenetic MarkersHematopoietic Stem CellsMaleMiceMice, Inbred C57BLRNA, Long NoncodingGenetic MarkersRNA, Long NoncodingRNA, UntranslatedXIST non-coding RNA

Identifiers

PMID16980619
PMCPMC1592878
OpenAlexW2172273789

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.