ARY ble and cell-bound forms of steel fa nocyte precursor dispersal and su ation pathway

In the trunk of vertebrate embryos, neural crest cells segregate from the neural epithelium and transiently reside in a ‘migrating staging area’ (MSA) delimited by the neural tube, the somite and the overlying epithelium. Crest cells immediately begin to disperse from the MSA on a ventromedial pathway along the myotome and into rostral sclerotomal mesenchyme (Erickson and Loring, 1987; Weston, 1991). Later, crest cells remaining in the MSA disperse on a dorsolateral pathway, migrating between the dermatome and the epidermis (Erickson et al., 1992). The crest cells on the lateral pathway subsequently become interspersed with dermal mesenchyme and cross the epithelial basement membrane to localize in the epidermis. In the mouse, these cells remain in the epithelium for many days before they undergo melanogenesis postnatally. Before early markers for pigment cell precursors were available, the timing of melanocyte precursor dispersal and localization in the skin was inferred by testing for the ability of cultured or grafted tissue to produce melanocytes (Rawles 19 fir of the embryonic trunk at about e11 and reach the limb buds by e12. At a lateral trunk level most of the melanocyte precursors enter the epidermis between e13 and e14 (Mayer, 1973). Recently, histochemical reagents that intensify pigment in melanosomes of otherwise undifferentiated melanocytes, or probes for melanocyte markers such as the tyrosine kinase receptor, c-kit, and tyrosinase-related protein-2 (TRP-2) confirmed these inferences, and revealed the presence of melanocyte precursors in the head as early as e10.5 (Manova and Bachvarova, 1991; Steel et al., 1992; Pavan and Tilghman, 1994). Several mouse mutations affecting coat pigmentation have been described and their molecular defects characterized. Two of the best studied, Steel (Sl) and Dominant spotting (W), are embryonic lethals as homozygotes, due to failure of erythropoiesis, whereas heterozygous embryos are viable but eventually show a white spotting coat color pattern. The defective gene in W mutants codes for a receptor tyrosine kinase (c-kit; Developm Printed in

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