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Kit and foxd3 genetically interact to regulate melanophore survival in zebrafish
Author(s) -
Cooper Cynthia D.,
Linbo Tor H.,
Raible David W.
Publication year - 2009
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.21910
Subject(s) - melanophore , biology , zebrafish , morpholino , mutant , tunel assay , microbiology and biotechnology , chromatophore , programmed cell death , receptor tyrosine kinase , immunoprecipitation , terminal deoxynucleotidyl transferase , phenotype , apoptosis , signal transduction , genetics , cell culture , gene
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.