| Previous | Next |
Although Mintz's interpretations of allophenic patterns have been criticized (e.g., Mystkowska and Tarkowski, 1968; McLaren and Bowman, 1969; Lyon, 1968, 1970, 1972a, Schaible 1972), 4 they are consistent with almost everything that is known about the behavior of pigment cells. Moreover, they are especially attractive because they readily explain the patterns displayed by single genotype mice. Thus, if one assumes that mechanisms are available in normal mice which are capable of producing melanoblast or hair follicle clones that differ phenotypically from each other, all of the pigment patterns of these animals appear to conform either to the archetypal or to the modified pigment patterns observed in allophenic subjects ( Mintz, 1971a). That such an assumption is not difficult to accept derives from the fact that some pigment patterns of ordinary mice have in fact been shown to be due to the occurrence of different clonal populations. Such clones, which are known as "phenoclones" (see Mintz, 1971c), are exemplified best in the pigment patterns of animals bearing an X-linked coat-color determinant. However, before dealing with these patterns, let us refocus on some of the autosomally associated bicolored patterns already considered to see if they can be interpreted in terms of the phenoclonal expression of allophenic patterns.
When the effects of the various p-locus alleles were discussed it was noted that there was one allele at this locus, known as p-unstable ( pun), which, when homozygous, produces a phenotype in which both dilute ( p/p) and intensely pigmented ( P/—) areas occur (see Chapter 4, Section II, C, 9). It was noted also that this bicolored pattern was very variable and that it seemed to be due to a spontaneous somatic reversion to wild type ( Melvold, 1971). An examination of many pun/pun mice clearly indicates that their pigment patterns conform to the patterns of two-color allophenics and that their spots are essentially abbreviated parts of transverse bands. In fact, the most highly patterned pun/pun mice are indistinguishable from allophenic mice displaying maximal differentiation among melanoblast bands ( Mintz, 1970). Clearly, as a result of somatic mutation(s) two populations of primordial cells have been produced in these mice and the behavior of these populations is exactly what one would predict from their behavior in the allophenic animal ( Figure 7-5).
Two other alleles at the p-locus, pm1 (pink-eyed mottled-1) and pm2 (pink-eyed mottled-2), when heterozygous with p also produce phenotypes which from their descriptions (see Chapter 4, Section II, C, 8) are like those in pun/pun mice and consequently mimic the melanoblast clonal patterns of allophenic animals. Although there is no evidence that somatic mutation is responsible for the reversion to intense pigmentation in these genotypes ( L. Russell, 1964), whatever that mechanism is, it appears to produce two phenoclones which again behave as Mintz's hypothesis predicts.
Chinchilla-mottled ( cm/cm) mice (see Chapter 3, Section II, B, 7) apparently are also characterized by patterns which resemble those of allophenic mice and, therefore, almost surely are produced via a similar mechanism.
The bicolored patterns produced by other autosomally inherited coat-color factors mimic the hair follicle clonal patterns of allophenics and this is consistent with their known activity in the hair bulb. Some of these examples involve a-locus alleles. Thus, viable yellow ( Avy/a) (see Chapter 2, Section I, A, 2), mottled agouti ( am/am) ( Chapter 2, Section I, A, 12), and agouti suppressor ( As Aw/AsAw) ( Chapter 2, Section I, A, 17) all produce phenotypes which are included in the array of patterns seen in allophenics derived from embryos of different a-locus constitutions ( Figure 7-6) ( Mintz, 1971a). Another coat-color determinant which may behave similarly is silver ( si/si) ( Mintz, 1971a) (see Chapter 6, Section II).
While some heterozygous bicolored phenotypes (e.g., pm1/p, Avy/a, cm/cch) could be due to the activity of one or the other allele in each cell, this does not seem to be a likely mechanism for the phenoclonal origin of most of the alleles with which we are dealing since many of them (e.g., Avy, am, cm) produce mottled phenotypes when homozygous. Nevertheless, this in no way invalidates the Mintz hypothesis since there is no reason to assume that the phenoclones of single genotype mice are all produced via the same mechanism. Indeed, we already have noted that whereas in pun/pun animals somatic mutation is responsible for the two populations of cells, this is not the case in pm1/p mice ( L. Russell, 1964).
| Previous | Next |