Genetic Analysis of Melanophore Development in Zebrafish Embryos

• DOI: 10.1006/dbio.2000.9840
• Publication Date: 2002-09-16T11:45:48Z
• Authors: Robert N. Kelsh; Bettina Schmid; Judith S. Eisen
• Keywords: melanophore; 0301 basic medicine; Embryo, Nonmammalian; proliferation; Molecular Sequence Data; Melanophores; survival; Gene Expression Regulation, Enzymologic; 03 medical and health sciences; Animals; Humans; Amino Acid Sequence; Cloning, Molecular; Molecular Biology; Zebrafish; Body Patterning; Danio rerio; dopachrome tautomerase; Sequence Homology, Amino Acid; Reverse Transcriptase Polymerase Chain Reaction; Gene Expression Regulation, Developmental; differentiation; Cell Biology; Recombinant Proteins; Intramolecular Oxidoreductases; specification; Neural Crest; pigment pattern formation; tyrosinase-related protein-2; neural crest; Sequence Alignment; Developmental Biology

Vertebrate pigment cells are derived from neural crest, a tissue that also forms most of the peripheral nervous system and a variety of ectomesenchymal cell types. Formation of pigment cells from multipotential neural crest cells involves a number of common developmental processes. Pigment cells must be specified; their migration, proliferation, and survival must be controlled and they must differentiate to the final pigment cell type. We previously reported a large set of embryonic mutations that affect pigment cell development from neural crest (R. N. Kelsh et al., 1996, Development 123, 369-389). Based on distinctions in pigment cell appearance between mutants, we proposed hypotheses as to the process of pigment cell development affected by each mutation. Here we describe the cloning and expression of an early zebrafish melanoblast marker, dopachrome tautomerase. We used this marker to test predictions about melanoblast number and pattern in mutant embryos, including embryos homozygous for mutations in the colourless, sparse, touchdown, sunbleached, punkt, blurred, fade out, weiss, sandy, and albino genes. We showed that in homozygous mutants for all loci except colourless and sparse, melanoblast number and pattern are normal. colourless mutants have a pronounced decrease in melanoblast cell number from the earliest stages and also show poor melanoblast differentiation and migration. Although sparse mutants show normal numbers of melanoblasts initially, their number is reduced later. Furthermore, their distribution indicates a defect in melanoblast dispersal. These observations permit us to refine our model of the genetic control of melanophore development in zebrafish embryos.