PUBLICATION

colgate/hdac1 repression of foxd3 expression is required to permit mitfa-dependent melanogenesis

Authors
Ignatius, M.S., Moose, H.E., El-Hodiri, H.M., and Henion, P.D.
ID
ZDB-PUB-071219-5
Date
2008
Source
Developmental Biology   313(2): 568-583 (Journal)
Registered Authors
Henion, Paul, Ignatius, Myron
Keywords
Neural crest, Melanophore, Histone deacetylase1, foxd3, mitfa, c-kit, Zebrafish
MeSH Terms
  • Models, Biological
  • Base Sequence
  • Binding Sites
  • Microinjections
  • Neural Crest/cytology
  • Neural Crest/embryology
  • Microphthalmia-Associated Transcription Factor/metabolism*
  • Electrophoretic Mobility Shift Assay
  • Gene Expression Regulation, Developmental*
  • Animals
  • In Situ Hybridization
  • Embryo, Nonmammalian
  • Promoter Regions, Genetic
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish/physiology*
  • Protein Binding
  • Histone Deacetylase 1
  • Mutation
  • Melanophores/cytology
  • Melanophores/metabolism
  • Melanophores/physiology
  • Forkhead Transcription Factors/metabolism*
  • Histone Deacetylases/genetics
  • Histone Deacetylases/metabolism
  • Histone Deacetylases/physiology*
  • Cell Movement
  • Molecular Sequence Data
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • Zebrafish Proteins/physiology*
  • Oligonucleotides, Antisense/pharmacology
(all 33)
PubMed
18068699 Full text @ Dev. Biol.
Abstract
Neural crest-derived pigment cell development has been used extensively to study cell fate specification, migration, proliferation, survival and differentiation. Many of the genes and regulatory mechanisms required for pigment cell development are conserved across vertebrates. The zebrafish mutant colgate (col)/histone deacetylase1 (hdac1) has reduced numbers, delayed differentiation and decreased migration of neural crest-derived melanophores and their precursors. In hdac1(col) mutants normal numbers of premigratory neural crest cells are induced. Later, while there is only a slight reduction in the number of neural crest cells in hdac1(col) mutants, there is a severe reduction in the number of mitfa-positive melanoblasts suggesting that hdac1 is required for melanoblast specification. Concomitantly, there is a significant increase in and prolonged expression of foxd3 in neural crest cells in hdac1(col) mutants. We found that partially reducing Foxd3 expression in hdac1(col) mutants rescues mitfa expression and the melanophore defects in hdac1(col) mutants. Furthermore, we demonstrate the ability of Foxd3 to physically interact at the mitfa promoter. Because mitfa is required for melanoblast specification and development, our results suggest that hdac1 is normally required to suppress neural crest foxd3 expression thus de-repressing mitfa resulting in melanogenesis by a subset of neural crest-derived cells.
Genes / Markers
Figures
Figure Gallery (12 images) / 2
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
b382
    Point Mutation
    zdf10
      Small Deletion
      1 - 2 of 2
      Show
      Human Disease / Model
      No data available
      Sequence Targeting Reagents
      Target Reagent Reagent Type
      foxd3MO3-foxd3MRPHLNO
      1 - 1 of 1
      Show
      Fish
      Antibodies
      No data available
      Orthology
      No data available
      Engineered Foreign Genes
      No data available
      Mapping
      No data available