The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel 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 steel homozygotes and severely reduced in steel Dickie and steel 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.
Although homozygous KitlSl-d/KitlSl-d have been described as being viable, Dr. Jane Barker of The Jackson Laboratory has found that in her colony B6.D2-KitlSl-d homozygotes die at birth or soon thereafter.

Mice homozygous for the spontaneous mutation kit ligand; steel Dickie (KitlSl-d) are viable, black-eyed white, usually sterile in one or both sexes, and have severe macrocytic anemia. This phenotype is also seen in heterozygous combinations of Steel Dickie with other steel alleles such as KitlSl/KitlSl-d.

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