Deletion of mouset-complex distorter-1 produces an effect like that of thet-form of the distorter

Abstract

SummaryAn allele of the mouse brachyury locus,T22H, had been shown previously to involve a deletion of several markers in the proximal part of chromosome 17, and almost certainly includes deletion of thet-complex distorter geneTcd-1. The effects ofT22Hon transmission ratio distortion and male sterility caused by thet-complex were compared with those of a partialt-haplotypeth51, which carries the t-form of the distorterTcd-1t. In combination with the complete haplotypetf32,T22Hcaused severe impairment of male fertility, but males of genotypeT22H/t6orT22H/thSlwere normally fertile. These results were very similar to those obtained whenth51was in combination with the same haplotypes. In effect on transmission ratioT22Hwas again similar tothSI, in that it produced a marked increase in the transmission of the haplotypet6. To test whether the effects ofT22Hwere due to deletion of elements other thanTcd-1, the effect ofT22Hon transmission of the partial haplotypeth2was compared with that of the deletionThv. AgainT22Hmarkedly increased transmission of the t-haplotype and the effect was significantly greater than the small effect produced byThp.It is concluded that deletion of the distorterTcd-1has an effect like that of thet-form of this distorter,Tcd-1t, and hence that Ted-11 must be an amorph or hypomorph. It is speculated that othert-complex distorters,Tcd-2tandTcd-3tmay also be amorphs or hypomorphs. Thus, the phenomena of transmission ratio distortion and male sterility due to thet-complex appear to be brought about by differential susceptibility of wild-type andt-responder alleles,Tcr+andTcrt, to a shortage of distorter gene product.