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
-
- Animals
- Base Sequence
- Binding Sites
- Cell Movement
- Electrophoretic Mobility Shift Assay
- Embryo, Nonmammalian
- Forkhead Transcription Factors/metabolism*
- Gene Expression Regulation, Developmental*
- Histone Deacetylase 1
- Histone Deacetylases/genetics
- Histone Deacetylases/metabolism
- Histone Deacetylases/physiology*
- In Situ Hybridization
- Melanophores/cytology
- Melanophores/metabolism
- Melanophores/physiology
- Microinjections
- Microphthalmia-Associated Transcription Factor/metabolism*
- Models, Biological
- Molecular Sequence Data
- Mutation
- Neural Crest/cytology
- Neural Crest/embryology
- Oligonucleotides, Antisense/pharmacology
- Promoter Regions, Genetic
- Protein Binding
- Zebrafish/embryology
- Zebrafish/genetics
- Zebrafish/metabolism
- Zebrafish/physiology*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- Zebrafish Proteins/physiology*
- PubMed
- 18068699 Full text @ Dev. Biol.
Citation
Ignatius, M.S., Moose, H.E., El-Hodiri, H.M., and Henion, P.D. (2008) colgate/hdac1 repression of foxd3 expression is required to permit mitfa-dependent melanogenesis. Developmental Biology. 313(2):568-583.
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
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping