期刊
MECHANISMS OF DEVELOPMENT
卷 123, 期 1, 页码 24-30出版社
ELSEVIER
DOI: 10.1016/j.mod.2005.10.005
关键词
histone deacetylase; oligodendrocyte; zebrafish; hedgehog; nkx2.2a; olig2
资金
- NINDS NIH HHS [R01-NS42925] Funding Source: Medline
- Medical Research Council [G0400100B] Funding Source: researchfish
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS042925] Funding Source: NIH RePORTER
Histone deacetylases are critical components of transcriptional silencing mechanisms that regulate embryonic development. Recent work has shown that histone deacetylase 1 (hdac1) is required for neuronal specification during zebrafish CNS development. We show here that specification of oligodendrocytes, the myelinating cells of the CNS, also fails to occur in the hdac1 mutant hindbrain, but persistence of neural progenitors in the hindbrain ventricular zone, which express pax6a and sox2, is independent of hdac1 activity. Commitment of ventral neural progenitors to the oligodendrocyte fate is thought to require co-ordinate, hedgehog-dependent expression of olig2 and nkx2.2a in these cells, leading to expression of sox10 and subsequent differentiation of oligodendrocytes. Remarkably, transcription of olig2 is extinguished in ventral neural progenitors of the hdac1 mutant hindbrain, whereas expression of nkx2.2a is up-regulated in these cells, and sox10 expression is suppressed. Our results identify hdac1 as a novel, essential component of the mechanism that allocates neural progenitors to the oligodendrocyte fate, by attenuating expression of a subset of neural progenitor genes and rendering olig2 expression responsive to Hedgehog signalling. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
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