Complex That Affect the Tail

A new recessive mutation affecting tail length is described. It is unlinked to the Tlt-complex on chromosome 17 and yet it shows cumulative phenotypic effects with several t-complex mutations: T, TCu, tct and Fu". It does not interact with five different nonchromosome I7 mutations that affect tail length. Thus, t-int is a tail modifier with surprisingly specific interactions. HE proximal part of the t-complex on chromoT some I7 in the mouse contains two genes known to affect tail length (ARTZT, BENNETT and SHIN 1985). One is the semidominant Bruchyury mutation (T) which causes a short tail in heterozygotes and is lethal at midgestation in homozygotes. The other mutation tct (the "tail interaction" factor formerly called t-int and t T ) is present only in t-haplotypes and, curiously, by itself has no phenotype in the heterozygous or homozygous condition. It is recognized by virtue of its interaction with T to produce tailless mice in compound heterozygotes (Tltct). In a formal sense, these two genes behave as alleles since they segregate from one another without recombination; however, since all naturally occurring tct factors exist within an inversion (HERRMANN et al. 1986) it is not known whether T and tct are unilocal. Both the short tailed and the tailless phenotypes are very sensitive to modifiers of tail length in the genetic background. For example, on the BALB/c background genetically short-tailed mice (T/+) tend to have very short tails, no more than one-third normal length, are frequently completely tailless and occasionally show spina bifida, while genetically tailless mice (T/ tc t ) often lack some sacral vertebrae, and may have severe spina bifida aperta. On the C3H background, on the other hand, T/+ mice have tails that are often 9/10 of normal length, and frequently overlap with normal. The number of the background modifiers in these strains is not known, nor have any been specifically identified. We report here the serendipitous discovery of a very specific modifier gene which does not appear to be linked to chromosome 17. We have called the new gene t-int since it appears to be unlinked to the t-complex. This symbol was previously used for the mutation now designated tct, but was discarded Present address: Department of Zoology, The University of Texas at Austin, Austin, Texas 78712. Genetics 116 601-605 (August, 1987) when the nomenclature committee decided that all tlinked tail interactive genes are to be called tct. Alone in heterozygotes or homozygotes t-int has no phenotype but has surprisingly discrete interactions with both tct and T, and also Fuki, another tail mutation located in the T/t complex. It does not interact with several other dominant and recessive tail mutations located on other chromosomes.