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.