Journal article
Kit and foxd3 genetically interact to regulate melanophore survival in zebrafish
Developmental dynamics, Vol.238(4), pp.875-886
04/2009
Handle:
https://hdl.handle.net/2376/109638
PMCID: PMC2730777
PMID: 19301400
Abstract
We have investigated the role of foxd3 activity in conjunction with signaling by the kit tyrosine kinase receptor in zebrafish black pigment cell (melanophore) development. As loss‐of‐function of these molecules individually has distinct effects on melanophore number, we have examined the phenotype of double mutants. Individuals with a null mutation in kit have fewer melanophores than wild‐type, with cells lost through death. When kit mutants are injected with foxd3 antisense morpholino oligonucleotides or crossed with a foxd3 zebrafish mutant, they have more melanophores than their uninjected or foxd3+ counterparts. Examination of foxd3 loss‐of‐function in two additional kit mutants that differentially alter kit‐dependent migration and survival indicates a change in melanophore number in survival mutants only. Consistently, TUNEL (terminal deoxynucleotidyl transferase–mediated deoxyuridinetriphosphate nick end‐labeling) analysis confirms a partial rescue of melanophores from cell death. Ectopic expression of foxd3 indicates that foxd3 promotes early melanophore death only when kit is inactive. Taken together, these data suggest a kit‐dependent role for foxd3 in the regulation of melanophore survival. Developmental Dynamics 238:875–886, 2009. © 2009 Wiley‐Liss, Inc.
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Details
- Title
- Kit and foxd3 genetically interact to regulate melanophore survival in zebrafish
- Creators
- Cynthia D CooperTor H LinboDavid W Raible
- Publication Details
- Developmental dynamics, Vol.238(4), pp.875-886
- Academic Unit
- Molecular Biosciences, School of
- Publisher
- Wiley‐Liss, Inc; New York
- Number of pages
- 12
- Grant note
- National Institutes of Health (1F32 HD047108‐01; 1R01‐NS45246)
- Identifiers
- 99900547360401842
- Language
- English
- Resource Type
- Journal article