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Dev Dyn. 2009 Apr;238(4):875-86. doi: 10.1002/dvdy.21910.

Kit and foxd3 genetically interact to regulate melanophore survival in zebrafish.

Author information

1
Department of Biological Structure, University of Washington, Seattle, Washington, USA. cdcooper@vancouver.wsu.edu

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.

PMID:
19301400
PMCID:
PMC2730777
DOI:
10.1002/dvdy.21910
[Indexed for MEDLINE]
Free PMC Article

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