THE CELLULAR BASIS FOR INTERACTION OF STERILITY FACTORS IN THE MOUSE T-HAPLOTYPE

The t haplotypes are variant forms of the proximal one-third of chromo some 17 in the mouse. They contain four inversions (relative to the wi ldtype DNA) extending over most of this region and house a number of m ale sterility factors. Males carrying two complete t haplotypes (t/t) are sterile, as are males homozygous for S2, the sterility factor loca ted in the most distal (relative to the centromere) inversion. Males h omozygous for the sterility factor S1, located in the most proximal in version, are not sterile; however, if such a male also is heterozygous for other sterility factors, then sterility results. It has been sugg ested therefore that homozygosity for S1 enhances the detrimental acti on of other sterility factors. Sperm from t/t males have severe motili ty defects and are unable to penetrate investment-free eggs, while spe rm from fertile t/+ mice have less serious motility defects and exhibi t a delay in penetration of investment-free eggs. To determine whether homozygosity for S1 enhances the cellular defects exhibited by sperm from mice heterozygous for other sterility factors, we compared the mo tility and egg-penetrating ability of sperm from fertile mice homozygo us for S1 to that of sperm from mice carrying one complete t haplotype and one proximal or distal partial t haplotype. The data suggest that sperm from males carrying a proximal partial t haplotype and a comple te t haplotype have serious defects in motility and penetration of the investment-free egg, and support the hypothesis that S1 enhances the detrimental effects of other sterility factors within the t haplotype.