[The expression of the mutant gene mi in mouse aggregation chimeras].

Using aggregation of 8-cell embryos belonging to two mouse strains, we produced 17 chimeras, mi/mi<==>+/+ (3 organisms), mi/+<==>+/+ (9 organisms), and +/+<==>+/+ (5 organisms), that achieved the age of 30 days. Chimerism was identified by mosaic pigmentation of coat and retinal pigment epithelium (RPE). All mi/mi<==>+/+ chimeras suffered from microphthalmia. Disturbances of eye development in these mice were similar to those in mi/mi animals. In all three chimeras, pigmentation of RPE and choroid was represented with alternating pigmented and depigmented patches. Mosaic RPE pattern probably resulted from the effects of para-orbital mesenchyme cells of different genotypes, +/+ or mi/mi. These findings confirm our earlier data that mutant alleles of the mi locus affect ectomesenchyme (neural crest) cells playing an important role in normal RPE development. Coat pigmentation in mi/mi<==>+/+ chimeras had the same spotted pattern as in mi/+ heterozygous mice. Hence, the gene mi functions in melanoblasts, but dermal and epidermal mi/mi cells do not suppress migration, proliferation, and differentiation of +/+ melanoblasts. The mi/mi dermal cells do not interfere with the expression of the gene A. Despite the high proportion of mi/mi cells (58 to 80%), bone resorption and eruption of teeth in mi/mi<==>+/+ chimeras proceeded as in normal animals.