PUBLICATION
Histone deacetylase 1 is essential for oligodendrocyte specification in the zebrafish CNS
- Authors
- Cunliffe, V.T., and Casaccia-Bonnefil, P.
- ID
- ZDB-PUB-051214-3
- Date
- 2006
- Source
- Mechanisms of Development 123(1): 24-30 (Journal)
- Registered Authors
- Cunliffe, Vincent
- Keywords
- Histone deacetylase, Oligodendrocyte, Zebrafish, Hedgehog, nkx2.2a, olig2
- MeSH Terms
-
- Stem Cells/cytology
- Stem Cells/enzymology
- Oligodendroglia/cytology
- Oligodendroglia/enzymology*
- Nerve Tissue Proteins/genetics
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish/metabolism*
- Animals
- In Situ Hybridization
- Cell Differentiation
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- Homeodomain Proteins/genetics
- Central Nervous System/cytology
- Central Nervous System/embryology*
- Central Nervous System/enzymology*
- Histone Deacetylases/genetics
- Histone Deacetylases/metabolism*
- Transcription Factors/genetics
- Histone Deacetylase 1
- Rhombencephalon/cytology
- Rhombencephalon/embryology
- Rhombencephalon/enzymology
- Basic Helix-Loop-Helix Transcription Factors/genetics
- Gene Expression Regulation, Developmental
- PubMed
- 16324829 Full text @ Mech. Dev.
Citation
Cunliffe, V.T., and Casaccia-Bonnefil, P. (2006) Histone deacetylase 1 is essential for oligodendrocyte specification in the zebrafish CNS. Mechanisms of Development. 123(1):24-30.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping