HDAC1 and HDAC2 regulate oligodendrocyte differentiation by disrupting the β-catenin–TCF interaction View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2009-07

AUTHORS

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, Jenny Hsieh, Rhonda Bassel-Duby, Eric N Olson, Q Richard Lu

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. More... »

PAGES

829-838

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nn.2333

DOI

http://dx.doi.org/10.1038/nn.2333

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1006528138

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19503085


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