Soft coat homozygotes have sparse, slightly curled vibrissae, and the fur is initially sparse and tufted and then becomes ruffled and untidy, although all four hair types are present. The hair follicle bulb is shorter and more rounded than normal, medullary cells are irregularly arranged, and the epidermis does not thin by 7 days of age, but is delayed in thinning until 10 or 12 days of age. The genetic impairment of this spontaneous mutation remains to be defined.Read More +
At birth, soft coat homozygotes have sparse, slightly curled whiskers and this feature persists in the adult. The hair follicle bulb is shorter, and more rounded than normal, there is a slight delay in the formation of the hair canal and in the eruption of the first coat. The initial coat can be sparse and grow in uneven tufts relative to heterozygotes, and then appear increasingly ruffled and untidy, with the hair standing out instead of laying in an organized pelt. All four hair types are present, but very thin, and the overhairs are more septate than normal. The medullary cells are irregularly arranged and elongate along the axis of the shaft more than normal. The epidermis does not thin by 7 days of age, but rather remains thick until 10 to 12 days of age. Grunenburg (1971) found no significant defect in the juxtaoral organ of Chievitz in soft coat homozygotes. Sundberg et al. (1997) found that soft coat homozygotes have a high tumor induction rate in response to 25 ug DMBA followed by 4 ug TPA applied to the dorsal thoracolumbar skin.
The softcoat (soc) mutation arose spontaneously in the BALB/cJ inbred strain at The Jackson Laboratory in 1966. It was outcrossed to C57BL/6J and bred homozygote x homozygote for 5 generations. Then it was backcrossed to C57BL/6J to N4 followed by sibling inbreeding with forced heterozygosis to N4F7 before outcrossing to C3FeLe.B6-a. The homozygous F2 from this cross-intercross was then crossed to the B6C3Fe-a/a F1 hybrid and the strain was maintained by cross-intercross with this hybrid. In 1986 this strain was cryopreserved at generation F32 using embryos from the cross of B6C3Fe-a/a F1 females with homozygous softcoat males.
|Gene Symbol and Name||a, nonagouti|
|Strain of Origin||old mutant of the mouse fancy|
|General Note||Insertion of the LV30 retrotransposon without the beta4 retrovirus sequence does not cause the nonagouti phenotype. J:278039|
|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 (beta4 retroviral sequence). 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.|
Some homozygotes may develop skin lesions.
When using the B6C3Fe a/a-soc/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #000240 in your Materials and Methods section.