Melanocytes originate from a small number of precursors localized either side of the dorsal midline. The tyrosine kinase receptor Kit and its ligand Mgf (Steel Factor) are essential for melanoblast survival and proliferation during their migration from the neural crest. Inappropriate Kit expression in the dermatome and dermis of patch and rump-white mouse mutants apparently sequester Mgf, inhibiting melanoblast dispersal. Using a reporter transgene Dct-lacZ, extensive regions of the mutant trunks appear devoid of melanoblasts between E12.5 and E15.5, a much larger area than seen in mutant adults. Melanoblast recolonization of the underpopulated lumbar regions occurs very rapidly by E16.5 giving rise to patterns consistent with those observed in adults. The mutations permit observation of aspects of melanoblast development that are not seen, or are obscured, in normal embryos.