Site of gene action in steel mice: Analysis of the pigment defect by mesoderm‐ectoderm recombinations

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Abstract
Mice homozygous for the gene steel (S1) are black‐eyed white, anemic and sterile. Previous studies have shown that the pigment defect in the skin and hair results from a failure of the tissue environment to support pigment cell development. In an attempt to analyse more critically this block of pigmentation by the skin, recombinations were made between dermal mesoderm and epidermal ectoderm from normal and mutant 13 day mouse embryos. The re‐combined skin pieces were then grown for 14 days in the chick coelom and subsequently examined for melanocytes in the dermis and epidermis. The results demonstrated that both the mesodermal and ectodermal components of steel skin are adversely affected by the mutant gene. Steel dermis combined with normal epidermis failed to receive or support the development of melanoblasts from the normal component. Steel epidermis combined with normal dermis likewise remained free of melanocytes. No effect of the steel components on the development of pigmentation in the normal associated component was observed. These results are discussed in relation to the general inhibition of pigment in tissues other than skin of steel mice, and in relation to the interesting pleiotropic effects of the gene steel.