ZFIN ID: ZDB-PUB-050518-18
Histone deacetylase 1 is required for cell cycle exit and differentiation in the zebrafish retina
Stadler, J.A., Shkumatava, A., Norton, W.H., Rau, M.J., Geisler, R., Fischer, S., and Neumann, C.J.
Date: 2005
Source: Developmental dynamics : an official publication of the American Association of Anatomists   233(3): 883-889 (Journal)
Registered Authors: Geisler, Robert, Neumann, Carl J., Norton, Will, Rau, Marlene J.
Keywords: cell cycle; differentiation; hdac1; retina; zebrafish
MeSH Terms:
  • Alleles
  • Animals
  • Cell Cycle*
  • Cell Differentiation*
  • Gene Expression Regulation, Developmental
  • Histone Deacetylase 1
  • Histone Deacetylases/deficiency
  • Histone Deacetylases/genetics
  • Histone Deacetylases/metabolism*
  • Retina/cytology*
  • Retina/embryology
  • Retina/enzymology*
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/deficiency
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 15895391 Full text @ Dev. Dyn.
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ABSTRACT
Histone acetylation is an important epigenetic mechanism for the control of eukaryotic transcription. The histone deacetylase 1 (HDAC1) gene has been implicated in controlling the transcription of core cell cycle regulators, but the in vivo role of HDACs in cell cycle regulation is still poorly understood. Loss of HDAC1 activity causes underproliferation in several contexts during vertebrate development. In contrast, we show here that HDAC1 has the opposite effect in the zebrafish visual system, where loss of HDAC1 activity leads to failure of cells to exit the cell cycle in the retina and in the optic stalk. The effect of HDAC1 on cell cycle exit is cell-autonomous, and loss of HDAC1 in the retina leads to up-regulation of cyclin D and E transcripts. These results demonstrate that the in vivo role of HDAC1 in regulating cell cycle progression is region-specific, as HDAC1 promotes cell cycle exit in the retina but stimulates proliferation in other cellular contexts. Developmental Dynamics, 2005. (c) 2005 Wiley-Liss, Inc.
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