Structural variants of the mouse Chr 17-specific t complex, known as t
haplotypes, express factors that alter the ability of sperm to carry
out their roles in the normal fertilization process. In previous studi
es of males carrying heterospecific combinations of the t complex, we
discovered a unique M. spretus/t haplotype phenotype of male sterility
. In additional studies with mice carrying a series of M. spretus-M. m
. domesticus recombinant Chr 17 homologs and a complete t haplotype (S
-+/t), we monitored physiological aspects of sperm function to map a l
ocus (Hst6) responsible for expression of the t-specific ''curlicue''
sperm flagellar curvature phenotype to 1 cM within the fourth inversio
n of the t complex. In the present report, we quantitatively analyze t
he in vitro capability of sperm from mice with similar S-+/t Chr 17 ge
notypes to fertilize zona pellucida-free mouse eggs. The results ident
ify a locus, Stop1, mapping distal to Pim1, with acute effects on the
ability of sperm to penetrate the oolemma. The data suggest that Stop1
is a complex locus consisting of at least two genetic elements, a pro
ximal one overlapping the Hst6 locus, and another, distal to the Hst6
locus. Further quantitative analyses of the ''curlicue'' phenotype pro
duced by sperm derived from these same animals indicate that expressio
n of this chronic flagellar curvature phenotype also derives from at l
east two elements, both mapping within the Hst6 locus. Thus, these stu
dies provide higher resolution mapping of the molecular basis of t hap
lotype-specific sperm dysfunction emanating from In(17)4.