Zebrafish Leucocyte tyrosine kinase controls iridophore establishment, proliferation and survival

Summary The zebrafish striped pattern results from the interplay among three pigment cell types; black melanophores, yellow xanthophores and silvery iridophores, making it a valuable model to study pattern formation in vivo. It has been suggested that iridophore proliferation, dispersal and cell sha...

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Published in:Pigment cell and melanoma research 2016-05, Vol.29 (3), p.284-296
Main Authors: Fadeev, Andrey, Krauss, Jana, Singh, Ajeet Pratap, Nüsslein-Volhard, Christiane
Format: Article
Language:English
Subjects:
Aging
Amino Acid Sequence
Animals
Base Sequence
Behavior, Animal
Body Patterning
Cell Communication
Cell Proliferation
Cell Survival
Chromatophores - cytology
Chromatophores - enzymology
homotypic competition
iridophores
leucocyte tyrosine kinase
Melanophores - cytology
Melanophores - metabolism
Mutation - genetics
Phenotype
pigment cells
Protein-Tyrosine Kinases - chemistry
Protein-Tyrosine Kinases - genetics
Protein-Tyrosine Kinases - metabolism
tumorigenesis
zebrafish
Zebrafish - metabolism
Zebrafish Proteins - chemistry
Zebrafish Proteins - genetics
Zebrafish Proteins - metabolism
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Summary:Summary The zebrafish striped pattern results from the interplay among three pigment cell types; black melanophores, yellow xanthophores and silvery iridophores, making it a valuable model to study pattern formation in vivo. It has been suggested that iridophore proliferation, dispersal and cell shape transitions play an important role during stripe formation; however, the underlying molecular mechanisms remain poorly understood. Using gain‐ and loss‐of‐function alleles of leucocyte tyrosine kinase (ltk) and a pharmacological inhibitor approach, we show that Ltk specifically regulates iridophore establishment, proliferation and survival. Mutants in shady/ltk lack iridophores and display an abnormal body stripe pattern. Moonstone mutants, ltkmne, display ectopic iridophores, suggesting hyperactivity of the mutant Ltk. The dominant ltkmne allele carries a missense mutation in a conserved position of the kinase domain that highly correlates with neuroblastomas in mammals. Chimeric analysis suggests a novel physiological role of Ltk in the regulation of iridophore proliferation by homotypic competition.
ISSN:1755-1471
1755-148X
DOI:10.1111/pcmr.12454