Evidence map›Paper›PMID 22589736›Full record

ArticlePLoS genetics2012

Histone h1 depletion impairs embryonic stem cell differentiation.

Yunzhe Zhang, Marissa Cooke, Shiraj Panjwani, Kaixiang Cao, Beth Krauth, Po-Yi Ho, Magdalena Medrzycki, Dawit T Berhe, Chenyi Pan, Todd C McDevitt and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 102 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Histone mutations in cancer.Biochemical Society transactions · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Epigenetic Regulation of Myogenesis: Focus on the Histone Variants.International journal of molecular sciences · 2021
    Review
  17. Article
  18. Article
  19. DOT1L-controlled cell-fate determination and transcription elongation are independent of H3K79 methylation.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  20. Article

7 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

11 authors at 2 institutions in 1 country.

Yunzhe ZhangSchool of Biology, Georgia Institute of Technology, Atlanta, Georgia, United States of America.
Marissa Cooke
Shiraj Panjwani
Kaixiang Cao
Beth Krauth
Po-Yi Ho
Magdalena Medrzycki
Dawit T Berhe
Chenyi Pan
Todd C McDevitt
Yuhong Fan
Georgia Institute of Technology · USThe Wallace H. Coulter Department of Biomedical Engineering · US

Funding

Role of Linker Histone H1 in Epigenetic Gene RegulationR01GM085261 · NIGMS · GEORGIA INSTITUTE OF TECHNOLOGY · PI FAN, YUHONG · 2008 to 2012
$2.0M
NIGMS NIH HHS GM085261NIGMS NIH HHS R01 GM085261PHS HHS CBET-0939511
6 · The paper itself

Abstract

Pluripotent embryonic stem cells (ESCs) are known to possess a relatively open chromatin structure; yet, despite efforts to characterize the chromatin signatures of ESCs, the role of chromatin compaction in stem cell fate and function remains elusive. Linker histone H1 is important for higher-order chromatin folding and is essential for mammalian embryogenesis. To investigate the role of H1 and chromatin compaction in stem cell pluripotency and differentiation, we examine the differentiation of embryonic stem cells that are depleted of multiple H1 subtypes. H1c/H1d/H1e triple null ESCs are more resistant to spontaneous differentiation in adherent monolayer culture upon removal of leukemia inhibitory factor. Similarly, the majority of the triple-H1 null embryoid bodies (EBs) lack morphological structures representing the three germ layers and retain gene expression signatures characteristic of undifferentiated ESCs. Furthermore, upon neural differentiation of EBs, triple-H1 null cell cultures are deficient in neurite outgrowth and lack efficient activation of neural markers. Finally, we discover that triple-H1 null embryos and EBs fail to fully repress the expression of the pluripotency genes in comparison with wild-type controls and that H1 depletion impairs DNA methylation and changes of histone marks at promoter regions necessary for efficiently silencing pluripotency gene Oct4 during stem cell differentiation and embryogenesis. In summary, we demonstrate that H1 plays a critical role in pluripotent stem cell differentiation, and our results suggest that H1 and chromatin compaction may mediate pluripotent stem cell differentiation through epigenetic repression of the pluripotency genes.

Indexed as

ChromatinEmbryonic Stem CellsHistonesAnimalsCell DifferentiationCells, CulturedDNA MethylationEmbryonic DevelopmentEpigenesis, GeneticGene Expression Regulation, DevelopmentalMiceNeuritesNeuronsOctamer Transcription Factor-3Promoter Regions, GeneticChromatinHistonesOctamer Transcription Factor-3Pou5f1 protein, mouse

Identifiers

PMID22589736
PMCPMC3349736
OpenAlexW2050489395

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.