The Sox18Ra and Sox18Ra-J alleles cause a less severe phenotype than the Sox18Ra-Op allele. The Sox18Ra and Sox18Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18Ra allele has been more broadly described in the literature and will be covered here. Heterozygotes are viable and fertile. Heterozygotes have developmentally retarded sinus hair growth apparent at embryonic day 16.5 and retarded development of pelage follicles apparent by embryonic day 17.5. Thus, heterozygotes have slightly shorter vibrissae evident at birth, and can be distinguished at three days of age by their pink skin which, due to the abnormally sparse development of the coat, fails to darken like that of wildtype siblings. A paucity of fur is apparent by nine days of age and persists throughout life. Compared with the wild type pelage, Sox18Ra/+ coats have l...
This strain is segregating for Sox18ra, Os, Pt, Es1a and Es1b.
The Sox18Ra and Sox18Ra-J alleles cause a less severe phenotype than the Sox18Ra-Op allele. The Sox18Ra and Sox18Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18Ra allele has been more broadly described in the literature and will be covered here. Heterozygotes are viable and fertile. Heterozygotes have developmentally retarded sinus hair growth apparent at embryonic day 16.5 and retarded development of pelage follicles apparent by embryonic day 17.5. Thus, heterozygotes have slightly shorter vibrissae evident at birth, and can be distinguished at three days of age by their pink skin which, due to the abnormally sparse development of the coat, fails to darken like that of wildtype siblings. A paucity of fur is apparent by nine days of age and persists throughout life. Compared with the wild type pelage, Sox18Ra/+ coats have longer guard hairs, shorter awls and zigzags, an increased number of guard hairs and awls, fewer zigzags, and no auchenes. There are mild morphological abnormalities in the hairs. There is no decrease in the number of hair follicles, but many of the follicles fail to grow hair. There is decreased yellow pigment in the hair causing the thin coat that develops to be darker than normal particularly in the dorsal midline. Subsequent to the first wave, hair growth is asynchronous and the normal cyclic fluctuations in skin thickness are not found. The adipose layer of the skin is thinner than normal. Despite this asynchrony of adjacent hair follicles, hair cycles do occur across the pelage, but are more diffuse than normal. The hair follicles have an aberrant shape and orientation. This aberrancy is more pronounced in homozygotes. The impact of the Sox18Ra mutation on hair is more pronounced in the anterior regions than in the posterior regions. Approximately one in ten heterozygous pups displays chylous ascites, and the most severely affected do not survive. This trait is seen in males more than in females and is modified by genetic background. (Carter and Phillips, 1954; Slee, 1956 and 1957; Mann, 1963; Herbertson and Wallace, 1964; Wallace, 1979.)
Homozygotes are nearly bald, lack vibrissae, and usually die before weaning. They have generalized edema and weigh more at birth than wildtype littermates. It has been estimated that 40% of homozygotes die as embryos. The homozygotes that survive are often 5-10% shorter in body length. There are fewer hair follicles than normal and the few hairs that do grow have abnormal morphology. There is pigment in the tail and ear pinnae, and theear pinnae are thinner than normal and are often wrinkled. (Carter and Phillips, 1954; Slee, 1956 and 1957; Mann 1963.)
Ragged (Sox18Ra) arose spontaneously in a cross bred stock at Edinburgh and was imported to the Jackson Laboratory about 1957. Oligosyndactyly (Os) arose in an irradiation experiment, probably X ray induced at Oak Ridge, in offspring of an F1 male from a 101 x C3H cross mated to a multiple recessive stock female. It was imported to the Jackson Laboratory from University College London in 1957. Pintail (Pt) arose at Yale Medical School at the 21st generation of inbreeding in a strain -30;pBr-30; (homozygous for a, Tyrpb, and p) after treatment with methylcholanthrene, and was imported to The Jackson Laboratory in the 1950-30;s. The linkage testing stock ROP/GnLe was established by Dr. M.C. Green by mating an Ra/+ female on a C57BL/6J congenic background to an Os/+ male in 1957. An Ra/+ Os/+ male was then mated to a B6.Cg-Pt heterozygous N11 female and the stock was within-stock bred for 8 generations. In 1959 inbreeding was started. It was then maintained by sibling matings only and cryopreserved in 1991 by mating Ra/+ Os/+ Pt/+ males to a normal non-mutant females at F80-82.
|Allele Type||Radiation induced|
|Gene Symbol and Name||Os, oligosyndactylism|
|Gene Synonym(s)||94-A; 94-K; PlmTgN(Pgk1)1Ddp; PlmTgN(Pgk1)1Ddp; PlmTgN(Pgk1)2Ddp; PlmTgN(Pgk1)2Ddp; postimplantation lethal mutation induced by Pgk1 transgene insertion-Dimitrina D. Pravtcheva 1; postimplantation lethal mutation induced by Pgk1 transgene insertion-Dimitrina D. Pravtcheva 2|
|Strain of Origin||(101 x C3H)F1|
|Gene Symbol and Name||Sox18, SRY (sex determining region Y)-box 18|
|Gene Synonym(s)||AI385749; HLTRS; HLTS; Ra; Ragl; Ragl; Sry-related HMG-box gene 18; expressed sequence AI385749; ragged; ragged-like|
|Strain of Origin||Translocation stock|
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