Journal
DEVELOPMENTAL BIOLOGY
Volume 313, Issue 2, Pages 568-583Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2007.10.045
Keywords
neural crest; melanophore; histone deacetylase1; foxd3; mitfa; c-kit; zebrafish
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Funding
- NEI NIH HHS [R01 EY015480, R01 EY015480-03, EY015480] Funding Source: Medline
- NIGMS NIH HHS [R01 GM076505] Funding Source: Medline
- NINDS NIH HHS [P30-NS045758, P30 NS045758, P30 NS045758-04] Funding Source: Medline
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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. (C) 2007 Elsevier Inc. All rights reserved.
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