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, compounds of two steel mutants (e.g. 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 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 adva...Read More +
|Allele Type||Gene Symbol||Gene Name|
|Allele Type||Gene Symbol||Gene Name|
|Allele Type||Gene Symbol||Gene Name|
|Allele Type||Gene Symbol||Gene Name|
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, compounds of two steel mutants (e.g. 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 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. This strain is also carrying the caracal-J (Krt71Ca-J) and hammer toe (Hm) mutations.
The linkage testing stock Hm, Sl, CaJ was developed from various stocks. It started with a dancer (Dc/+) male mated to a steel (Sl/+) female in 1959. Dancer originated as a spontaneous mutation at the Jackson Laboratory in the C3H/He-Lepob stock at N4 in 1956. Steel (KitlSl) arose spontaneously at the Jackson Laboratory in a C3H inbred strain and was maintained in a non-inbred multiple mutation stock by Dr. M.C. Green. A dancer steel (Dc/+ KitlSl/+) mouse was crossed once to strain C57BL/6J. A dancer steel off spring was crossed to a homozygous caracul (Ca/Ca) mouse from an inbred caracul stock of Dr. G. D. Snell. Caracul was an early mutation that arose in a Swiss stock in the 1930s. The caracul steel cross was sibling mated for 4 generations without dancer and at F4 a caracul steel heterozygote was mated to a twirler (Tw/+) male. Twirler arose spontaneously in the PCS multiple recessive stock at Harwell and was imported to the Jackson Laboratory in 1961. The caracul steel twirler stock (Ca/+ Sl/+ Tw/+) was maintained by sibling and non-sibling matings until 1967 when twirler was replaced with hammer toe (Hm). Hammer toe arose spontaneously at the Jackson Laboratory in a linkage cross in which luxate (lu) was segregating. The three mutations Ca, Sl, and Hm were maintained together and backcrossed to C57BL/6J for 5 generations. In 1969 at N5 sib matings were used and in 1971 caracul (Ca) was replaced with caracul Jackson (CaJ) which had arisen spontaneously in strain C57BL/6J. After several sibling matings with the 3 mutations segregating the Hm/+ Sl/+ CaJ/+ stock was backcrossed to C57BL/6J to N19. In 1977 a B6.Cg-Hm/+ Sl/+ CaJ/+ mouse at N19 was outcrossed to strain C3FeLe.B6-a/J and the strain was then maintained via continued backcrossing to strain C3FeLe.B6-a/J. It reached N76 in 1995. Embryos were generated for cryopreservation in 1989 by mating Hm/+ Sl/+ CaJ/+ mice to a C3FeLe.B6-a/J.
|Allele Synonym(s)||MgfSl; Sl|
|Gene Symbol and Name||Kitl, kit ligand|
|Gene Synonym(s)||Clo; Con; DCUA; DFNA69; FPH2; FPHH; Gb; Gb; KL-1; Kitlg; MGF; Mgf; Mgf; SCF; SF; SHEP7; SLF; Sl; Sl; Steel; Steel factor; blaze; blz; blz; cloud gray; contrasted; grizzle-belly; grizzle-belly; mast cell growth factor; steel; stem cell factor|
|Strain of Origin||C3H|
|Molecular Note||By Southern blotting, it was concluded that this allele contains a deletion encompassing most, if not all, of the coding region of the gene. A probe corresponding to nucleotides 6 to 685 of the cDNA failed to hybridize to DNA obtained from embryos homozygous for this allele. PCR analysis with primers for sequences at various distances from the Kit gene narrowed the 5' and 3' deletion endpoints to a 350 and a 380 base-pair region, respectively. Sequencing of the product of PCR using primers designed to span the deletion revealed that it extends through 973,366 base pairs on Chromosome 10 between nucleotide positions 99,177,807 and 100,151,173 (NCBI Map Viewer, Build 36.1), with a 4-base pair insertion joining the deletion endpoints, and contains 6 predicted and 3 known genes.|
|Allele Name||caracul Jackson|
|Gene Symbol and Name||Krt71, keratin 71|
|Gene Synonym(s)||AA589543; Ca; Ca; Cal4; Cal4; Cu; Cu; HYPT13; K6IRS1; KRT6IRS; KRT6IRS1; Krt2-6g; Krt2-6g; caracul; caracul-like 4; curly; expressed sequence AA589543; keratin complex 2, basic, gene 6g; mK6irs; mK6irs1|
|Strain of Origin||C57BL/6J|
|Molecular Note||Sequence analysis identified the spontaneous deletion of codon 140, comprised of nucleotides 418, 419, and 420 (CAA). The deleted codon predicted an asparagine in the alpha-helical rod domain. This molecular lesion is the same that has been identified in Krt2-6gCa-Rin, Ca9J, and Ca10J.|
|Gene Symbol and Name||a, nonagouti|
|Gene Synonym(s)||AGSW; AGTI; AGTIL; ASP; As; As; SHEP9; agouti; agouti signal protein; agouti suppressor|
|Strain of Origin||old mutant of the mouse fancy|
|Molecular Note||Characterization of this allele shows an insertion of DNA comprised of a 5.5kb virus-like element, VL30, into the first intron of the agouti gene. The VL30 element itself contains an additional 5.5 kb sequence, flanked by 526 bp of direct repeats. The host integration site is the same as for at-2Gso and Aw-38J and includes a duplication of four nucleotides of host DNA and a deletion of 2 bp from the end of each repeat. Northern analysis of mRNA from skin of homozygotes shows a smaller agouti message and levels 8 fold lower than found in wild-type.|
Krt71Ca-J, KitlSl and Hm are not linked and thus mice with various combinations of these mutations will be found from an Heterozygote x F1 breeding scheme.
When using the C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #000291 in your Materials and Methods section.
|Heterozygous or Wild-type for Krt71<Ca-J>, Heterozygous or Wild-type for Kitl<Sl>, Heterozygous or Wild-type for Hm|
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