Evidence map›Paper›PMID 19503085›Full record

ArticleNature neuroscience2009

HDAC1 and HDAC2 regulate oligodendrocyte differentiation by disrupting the beta-catenin-TCF interaction.

Feng Ye, Ying Chen, ThaoNguyen Hoang, Rusty L Montgomery, Xian-hui Zhao, Hong Bu, Tom Hu, Makoto M Taketo, Johan H van Es, Hans Clevers and 4 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Nature neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 347 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
347citing papers in PubMed, 1 pooled it
24.4field-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

347 citing papers in PubMed, 1 synthesis or guideline pooled it, 553 citations in OpenAlex.

  1. Pooled it
  2. Review
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  7. Article
  8. Article
  9. Review
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  11. Article
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  14. Review
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  16. Article
  17. Development of Oligodendroglia and Myelin.Advances in neurobiology · 2025
    Review
  18. Article
  19. Article
  20. Pan-ErbB inhibition impairs cognition via disrupting myelination and aerobic glycolysis in oligodendrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article

287 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 7 institutions in 4 countries.

Feng YeDepartment of Developmental Biology and Kent Waldrep Foundation Center for Basic Neuroscience Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, USA.
Ying Chen
ThaoNguyen Hoang
Rusty L Montgomery
Xian-hui Zhao
Hong Bu
Tom Hu
Makoto M Taketo
Johan H van Es
Hans Clevers
Jenny Hsieh
Rhonda Bassel-Duby
Eric N Olson
Q Richard Lu
The University of Texas Southwestern Medical Center · USHubrecht Institute for Developmental Biology and Stem Cell Research · NLFoundation Center · USKyoto University · JPSouthwestern Medical Center · USWest China Hospital of Sichuan University · CNWest China Second University Hospital of Sichuan University · CN

Funding

Olig2 in Oligodendrocyte Myelination and RemyelinationR01NS050389 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2005 to 2009
$1.8M
NINDS NIH HHS NS050389NINDS NIH HHS R01 NS050389
6 · The paper itself

Abstract

Oligodendrocyte development is regulated by the interaction of repressors and activators in a complex transcriptional network. We found that two histone-modifying enzymes, HDAC1 and HDAC2, were required for oligodendrocyte formation. Genetic deletion of both Hdac1 and Hdac2 in oligodendrocyte lineage cells resulted in stabilization and nuclear translocation of beta-catenin, which negatively regulates oligodendrocyte development by repressing Olig2 expression. We further identified the oligodendrocyte-restricted transcription factor TCF7L2/TCF4 as a bipartite co-effector of beta-catenin for regulating oligodendrocyte differentiation. Targeted disruption of Tcf7l2 in mice led to severe defects in oligodendrocyte maturation, whereas expression of its dominant-repressive form promoted precocious oligodendrocyte specification in developing chick neural tube. Transcriptional co-repressors HDAC1 and HDAC2 compete with beta-catenin for TCF7L2 interaction to regulate downstream genes involved in oligodendrocyte differentiation. Thus, crosstalk between HDAC1/2 and the canonical Wnt signaling pathway mediated by TCF7L2 serves as a regulatory mechanism for oligodendrocyte differentiation.

Indexed as

Cell DifferentiationAnimalsAstrocytesbeta CateninBrainCells, CulturedChick EmbryoFemaleHistone Deacetylase 1Histone Deacetylase 2Histone DeacetylasesMiceMice, TransgenicMotor NeuronsMutationOligodendrogliabeta CateninCTNNB1 protein, mouseHdac1 protein, mouseHdac2 protein, mouseHdac2 protein, ratHistone Deacetylase 1Histone Deacetylase 2Histone DeacetylasesRepressor ProteinsTcf7l2 protein, mouseTcf7l2 protein, ratTCF Transcription FactorsTranscription Factor 7-Like 2 ProteinWnt Proteins

Identifiers

PMID19503085
PMCPMC2701973
OpenAlexW2123453097

What OpenQuestion holds

Textmetadata
LicenceTDM
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.