HDAC1 and HDAC2 regulate oligodendrocyte differentiation by disrupting the β-catenin–TCF interaction
Open accessAbstract
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.
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HDAC inhibitors activate Wnt/β-catenin signaling in hippocampus-derived HCN cells and oligodendrocyte lineage cells.
“Secondly, while HDAC1/2 disrupts the β-catenin-TCF interaction and consequently suppresses the Wnt/β-catenin signaling pathway, and HDAC inhibitors activate Wnt/β-catenin signaling in the hippocampus-derived HCN cells and oligodendrocyte lineage cells [42].”
From CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease (2026) · cites this paper as [42]
In Results, “Stabilization of β-catenin in the absence of HDAC1/2” (page unavailable), TSA and valproic acid enhanced a Wnt/β-catenin reporter in hippocampus-derived HCN cells. The paper also reports Wnt activation after HDAC1/2 deletion in oligodendrocyte-lineage cells, but that does not establish that HDAC inhibitor treatment activated the pathway in those cells. (LLM, conf=0.85)
Experimental — accuracy not yet measuredTcf7l2 is involved in oligodendrocyte differentiation.
“Tcf7l2, involved in oligodendrocyte differentiation (15)”
From Oligodendrocyte heterogeneity in the mouse juvenile and adult central nervous system (2016) · cites this paper as [15]
Inhibition of class I HDACs is associated with activation of Wnt/β-catenin signaling.
“It has been demonstrated that inhibition of class I HDACs is associated with activation of Wnt/β-catenin signaling [42–47].”
From CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease (2026) · cites this paper as [42]
HDAC1/2 disrupts the β-catenin-TCF interaction and consequently suppresses the Wnt/β-catenin signaling pathway.
“Secondly, while HDAC1/2 disrupts the β-catenin-TCF interaction and consequently suppresses the Wnt/β-catenin signaling pathway, and HDAC inhibitors activate Wnt/β-catenin signaling in the hippocampus-derived HCN cells and oligodendrocyte lineage cells [42].”
From CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease (2026) · cites this paper as [42]
Depletion of HDAC1/2 stabilizes β-catenin and activates Wnt/β-catenin signaling in oligodendrocyte lineage cells.
“Firstly, depletion of HDAC1/2 stabilizes β-catenin and activates Wnt/β-catenin signaling in oligodendrocyte lineage cells [42].”
From CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease (2026) · cites this paper as [42]
A growing body of evidence shows that inhibition of class I HDACs results in activation of Wnt/β-catenin signaling.
“A growing body of evidence shows that inhibition of class I HDACs results in activation of Wnt/β-catenin signaling.”
From CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease (2026) · cites this paper as [42]
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- Authors
- Ye, F., Chen, Y., Hoang, T., Montgomery, R. L., Zhao, X.-H., Bu, H., Hu, T., Taketo, M. M., van Es, J. H., Clevers, H., Hsieh, J., Bassel-Duby, R., Olson, E. N., & Lu, Q. R.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- The University of Texas at Dallas (US)
- Sichuan University (CN)
- Kyoto University (JP)
- Hubrecht Institute for Developmental Biology and Stem Cell Research (NL)
- Corresponding author
- Lu, Q Richard
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2009-06-07
- Volume
- 12
- Issue
- 7
- Pages
- 829-838
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC2701973
- OpenAlex
- W2123453097
- Cited by
- 559
- References
- 52
- Citations by year
- 2026: 16 · 2025: 14 · 2024: 19 · 2023: 22 · 2022: 20 · 2021: 25 · 2020: 41 · 2019: 36 · 2018: 29 · 2017: 27 · 2016: 36 · 2015: 47 · 2014: 48 · 2013: 50 · 2012: 41
- FWCI
- 13.37
- Type
- journal article
- Language
- en
- Update notices
- correction (2025-07-16)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- KNAW research portal (Royal Academy of Art and Sciences (KNAW)) (publishedVersion)
- PubMed Central (acceptedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- KNAW Research Portal (The Royal Netherlands Academy of Arts and Sciences) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (NS050389, R01NS050389)
- National Institute of Child Health and Human Development
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- HDAC1, HDAC2, oligodendrocyte differentiation, Wnt/β-catenin signaling, β-catenin, TCF7L2, TCF4, corepressors, Olig2, histone deacetylase, neural tube development, oligodendrocyte precursor cells, transcriptional regulation
- MeSH terms
- Animals, Astrocytes, Brain, Cell Differentiation, Cells, Cultured, Chick Embryo, Female, Histone Deacetylases, Mice, Transgenic, Motor Neurons, Mutation, Oligodendroglia, Rats, Inbred F344, Repressor Proteins, Spinal Cord, Signal Transduction, Wnt Proteins, beta Catenin, Mice, Rats, TCF Transcription Factors, Histone Deacetylase 1, Histone Deacetylase 2, Transcription Factor 7-Like 2 Protein
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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