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The preceding chapters have been concerned almost entirely with the genetic control of melanin synthesis in melanocytes which are distributed uniformly, at least insofar as the coat is concerned. Attention now will be focused on genetic factors which can eliminate melanocytes either partially or completely.
Evidence already has been presented (see Chapter 3, Section II, A) which indicates that white spotting results from the complete absence of melanocytes from certain areas of the coat. The cause of these unpigmented areas in terms of Mintz's allophenic model has also been considered (see Chapter 7, Section VII). Thus, according to this model, all-white spotting results from the "preprogrammed" death of one or more melanoblast clones. There are, however, a number of other hypotheses which attempt to explain piebaldism. Although these will be discussed in the sections to which they most appropriately relate, the hypothesis proposed by Schaible ( 1969, 1972) deserves to be considered at this time since, like Mintz's, it proposes that all spotting patterns have a similar etiology.
Schaible contends that the complete pigmentation of mammals and birds develops from the expansion and merger of clones of pigment cells from the same centers that appear as pigmented spots against a white background in white spotted mutants. Employing different mouse mutations which cause white spotting but which are associated with nearly normal pigment coverage in certain parts of the body, such as belted ( bt/bt) and piebald ( s/s), either alone or in combination with other spotting factors, e.g., Miwh/+ (white) or Wa/+ (Ames dominant spotting), Schaible selected for progressive restriction of these pigmented areas until the center of each was located. Employing this method he was able to locate 14 such centers (see, however, Lyon and Glenister, 1971). He contends therefore that the integument of the mouse pigmented by the proliferation of 14 primordial melanoblasts which migrate from the neural crest and which locate themselves singly in bilateral centers in the nasal, temporal, aural, costal, lumbar, and sacral areas and in medial centers in the coronal and caudal areas (see Figure 9-1). 1 In fully pigmented mice these 14 clones proliferate and expand until they merge. However, in white spotted animals one or more of these clones fail to proliferate either entirely or completely. According to this model white spotted areas not only lack melanocytes but at no time are they populated with melanoblasts. Nevertheless, pigment cells can migrate into these areas secondarily from neighboring pigmented areas during postnatal growth.
While the method employed by Schaible to form this model was indeed and ingenious one, it does not seem to make as much biological sense as Mintz's. Unlike hers, which is completely in accord with Rawles' ( 1947) embryological observations, many of his clonal centers have absolutely no physical connection with the neural crest (see Mintz, 1974). Moreover, contrary to his hypothesis there is evidence (see note 11) that melanoblasts reach all areas of the integument in at least some white spotted genotypes ( Mayer, 1967a).
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