The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two MgfSl mutants (e.g. MgfSl/MgfSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable MgfSl/ MgfSl homozygotes and deficient in the MgfSl/+ heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age.
The Steel 16 Jackson mutation arose spontaneously in a stock derived from a 129 female crossed with a male of a wild-derived line originating from Lipari, Italy, which had been imported from Dr. Alfred Gropp into the laboratory of Dr. Eva Eicher at The Jackson Laboratory. This mutant subline was crossed once to B6D2, once to C57BL/6J and then twice to AEJ/GnRk and then maintained by sibling breeding thereafter, resulting in a nonagouti STOCK. In 1984 embryos were cryopreserved from C57BL/6J females bred to heterozygous males at generation F16.