Genetic analysis of melanophore development in zebrafish embryos

被引:155
作者
Kelsh, RN
Schmid, B
Eisen, JS
机构
[1] Max Planck Inst Entwicklungsbiol, Abt 3, D-72076 Tubingen, Germany
[2] Univ Oregon, Inst Neurosci, Eugene, OR 97403 USA
[3] Univ Bath, Dept Biol & Biochem, Bath BA2 7AY, Avon, England
关键词
melanophore; neural crest; specification; proliferation; survival; differentiation; pigment pattern formation; tyrosinase-related protein-2; dopachrome tautomerase; Danio rerio;
D O I
10.1006/dbio.2000.9840
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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. (C) 2000 Academic Press.
引用
收藏
页码:277 / 293
页数:17
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