Journal article
Transcription factor Ap-2α is necessary for development of embryonic melanophores, autonomic neurons and pharyngeal skeleton in zebrafish
Developmental biology, Vol.265(1), pp.246-261
2004
DOI: 10.1016/j.ydbio.2003.09.029
PMID: 14697367
Abstract
The genes that control development of embryonic melanocytes are poorly defined. Although transcription factor Ap-2α is expressed in neural crest (NC) cells, its role in development of embryonic melanocytes and other neural crest derivatives is unclear because mouse
Ap-2α mutants die before melanogenesis. We show that zebrafish embryos injected with morpholino antisense oligonucleotides complementary to
ap-2α (
ap-2α MO) complete early morphogenesis normally and have neural crest cells. Expression of
c-kit, which encodes the receptor for the Steel ligand, is reduced in these embryos, and, similar to zebrafish
c-kit mutant embryos, embryonic melanophores are reduced in number and migration. The effects of
ap-2α MO injected into heterozygous and homozygous
c-kit mutants support the notion that Ap-2α works through C-kit and additional target genes to mediate melanophore cell number and migration. In contrast to
c-kit mutant embryos, in
ap-2α MO-injected embryos, melanophores are small and under-pigmented, and unexpectedly, analysis of mosaic embryos suggests Ap-2α regulates melanophore differentiation through cell non-autonomous targets. In addition to melanophore phenotypes, we document reduction of other neural crest derivatives in
ap-2α MO-injected embryos, including jaw cartilage, enteric neurons, and sympathetic neurons. These results reveal that Ap-2α regulates multiple steps of melanophore development, and is required for development of other neuronal and non-neuronal neural crest derivatives.
Details
- Title: Subtitle
- Transcription factor Ap-2α is necessary for development of embryonic melanophores, autonomic neurons and pharyngeal skeleton in zebrafish
- Creators
- Erin K O'Brien - Department of Otolaryngology, University of Iowa College of Medicine, Iowa City, IA 52242, USAClaudia d'Alençon - Department of Anatomy and Cell Biology, University of Iowa College of Medicine, Iowa City, IA 52242, USAGregory Bonde - Department of Anatomy and Cell Biology, University of Iowa College of Medicine, Iowa City, IA 52242, USAWei Li - Department of Anatomy and Cell Biology, University of Iowa College of Medicine, Iowa City, IA 52242, USAJeff Schoenebeck - Departamento de Biologı́a, Facultad de Ciencias, Universidad de Chile, Santiago, ChileMiguel L Allende - Developmental Genetics Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016, USABruce D Gelb - Departments of Pediatrics and Human Genetics, Mount Sinai School of Medicine, New York, NY 10029, USADeborah Yelon - Departamento de Biologı́a, Facultad de Ciencias, Universidad de Chile, Santiago, ChileJudith S Eisen - Institute of Neuroscience, University of Oregon, Eugene, OR 97403, USARobert A Cornell - Department of Anatomy and Cell Biology, University of Iowa College of Medicine, Iowa City, IA 52242, USA
- Resource Type
- Journal article
- Publication Details
- Developmental biology, Vol.265(1), pp.246-261
- DOI
- 10.1016/j.ydbio.2003.09.029
- PMID
- 14697367
- NLM abbreviation
- Dev Biol
- ISSN
- 0012-1606
- eISSN
- 1095-564X
- Publisher
- Elsevier Inc
- Language
- English
- Date published
- 2004
- Academic Unit
- Anatomy and Cell Biology; Dental Research
- Record Identifier
- 9984025329702771
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