Dominant lethality of the mouse skeletal mutation tail-short (Ts) is determined by the Ts allele from mating partners.

Mice with the Tail-short (Ts) mutation have a short, kinky tail and numerous skeletal abnormalities, including a homeotic anteroposterior patterning problem involving the axial skeleton. The viability of Ts heterozygotes varies dramatically, depending on the mouse strain crossed with the mutant strain. At the extremes, the heterozygotes are viable or lethal prenatally. In this study, we found that laboratory mouse strains could be divided into two groups. A cross with strains from the first group yielded viable Ts heterozygotes, whereas a cross with the second group resulted in dominant lethality in utero. We planned to map the gene(s) that controls strain differences in the viability of the Ts heterozygotes. The result clearly indicated that a single chromosomal region, genetically inseparable from the Ts locus, is responsible for these differences. This suggests that allelism at the Ts locus generates variable manifestation of the mutant phenotype. Morphological and histological analyses indicated that embryos from the lethal cross exhibit severe developmental defects from the gastrulation stage through the early fetal stage. In particular, the umbilical vein does not develop properly. All of these results suggest that the phenotype of the Ts mutant is modified by the Ts alleles of the mating partners.