ZFIN ID: ZDB-PUB-001017-1
Genetic analysis of melanophore development in zebrafish embryos
Kelsh, R.N., Schmid, B., and Eisen, J.S.
Date: 2000
Source: Developmental Biology 225(2): 277-293 (Journal)
Registered Authors: Eisen, Judith S., Kelsh, Robert, Schmid, Bettina
Keywords: melanophore; neural crest; specification; proliferation; survival; differentiation; pigment pattern formation; tyrosinase-related protein-2; dopachrome tautomerase; Danio rerio
MeSH Terms: Amino Acid Sequence; Animals; Body Patterning; Cloning, Molecular; Embryo, Nonmammalian/cytology (all 23) expand
PubMed: 10985850 Full text @ Dev. Biol.
FIGURES   (current status)
ABSTRACT
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.
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