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Publication : T25H: a radiation-induced deletion affecting the T, qk and Tme loci

First Author  Fisher G Year  1992
Journal  Mouse Genome Volume  90
Issue  2 Pages  209-210
Mgi Jnum  J:1278 Mgi Id  MGI:49808
Citation  Fisher G, et al. (1992) T25H: a radiation-induced deletion affecting the T, qk and Tme loci. Mouse Genome 90(2):209-210
abstractText  Full text of Mouse Genome contribution: Research News: 1. T25H; a radiation-induced deletion affecting the T, qk and Tme loci. A male with a shortened, kinky tail was found among the progeny of a C3H/HeH x 101/H F1 hybrid female mouse given 1 Gy of acute X-rays. Breeding tests showed the phenotype was inherited as an autosomal dominant: of 93 offspring, 33 were classified as having abnormal tails. In all bar one animal the abnormal tails were shortened and blunt-ended, similar to the phenotype of brachyury (T); the exception had a vestigial tail. To test whether the mutation was allelic with brachyury, heterozygous males were mated to females of the genotype th2 tf/ lh2 tf. Twenty five of 55 offspring from this cross were tailless, as expected of a T/t combination. The mutation was therefore provisionally assumed to be allelic with brachyury, designated T25H, and further linkage matings set up to confirm its location. T25H + +/ th2 + tf males were mated to + qk tf/ + qk tf females. With the exception of one female (see below), T'25H + +/ + qk tf offspring of this cross displayed the quaking phenotype suggesting the mutation also involved the qk locus. The segregation of T25H and tf was classified in 57 offspring of this cross with the following results: T25H +/ + tf, 26; + tf/ + tf, 26; T25H tf/ + tf; 4; + +/ + tf, 1. Various matings involving T25H/+ females have been initiated. To date, 10 out of 93 offspring have been classified as carrying T25H; three of these were dead at birth, 6 died during the pre-weaning period, while 1 survived to 25 days. The mutation would therefore appear to be incapable of being transmitted successfully from heterozygous females, suggesting the mutation affects the Tme locus. The exceptional female from the cross described above involving qk was mated to a normal male. None of the 26 offspring she produced were T25H heterozygotes. However, as maternal transmission of T25H is clearly impaired, it was not possible to ascertain unequivocally whether this exceptional female actually carried the mutation or was an error of classification. T25H's effect on maternal transmission is reminiscent of that associated with Thp in which heterozygous carriers are generally dead at parturition although on rare occasions may survive to adulthood (M,F. Lyon, personal communication). Chromosome preparations were made from bone marrow cells of a T25H/+ male and from foetal livers of T25H / lh2 embryos. Initial observations on G-banded metaphases indicate a small deletion provisionally involving 17A3.2 and possibly 17A3.3. A recent re-examination of Thp has suggested there may be a small cytologically visible deletion in the same region of chromosome 17 (E.P. Evans, personal communication). T25H would therefore appear to be comparable in nature to Thp. (Fisher and Tease) (This work is supported by Euratom Contract Bi6- 143)
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