Homozygosity for the tail short mutation causes early embryonic lethality. Heterozygotes are smaller than normal and have variably shortened tails with flexures. Skeletal abnormalities are found with varying expressivity including vertebral fusions, bilateral asymmetry of the length of the humerus and tibia, triphalangy of digit 1 of the forefoot, an extra pair of ribs, and craniofacial defects. Embryonic anemia and reduced fertility are also found.
The Ts mutation arose spontaneously in 1946 at the National Cancer Institute in BALB/c (strain C of the Bagg albino strain) when that inbred was at generation F63. W.C. Morgan gave this mutant subline to George Snell at The Jackson Laboratory in 1950 and Snell outcrossed it to C57BL/6, C57BR/a, and BALB/cSn before inbreeding began on this new background and the line was transferred to Skippy Lane. The TSJ/Le inbred reached generation F41 in 1979 and F130 in 2007. When this inbred reached generation F132 it was backcrossed repeatedly to BALB/cJ and in 2010 sperm was cryopreserved from males heterozygous for Ts and Tyrc and homozygous for Tyrp1b then at generation N4. Cryorecovery using BALB/cJ females for in vitro fertilization has proven successful.
|Gene Symbol and Name||Rpl38, ribosomal protein L38|
|Strain of Origin||BALB/c|
|Molecular Note||An 18,189 kb region (from position 114,517 - 114,536 kb) was deleted and replaced with a 657 bp insertion showing high sequence similarity to the gag/pro-pol-dUTPase genes of the endogenous retrovirus MuERV-L. This deletion encompasses all of the exons of Rpl38.|
When using the tail-short mouse strain in a publication, please cite the originating article(s) and include JAX stock #011114 in your Materials and Methods section.