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Abstract
Mammalian seminal plasma is known to contain a
decapacitation factor(s) and to prevent capacitation and
thus fertility of sperm. This phenomenon has been observed
in experiments in vitro that assessed inhibition of
epididymal sperm fertility by seminal plasma or by the
purified decapacitation factor. However, the phenomenon of
the decapacitation has not yet been characterized in vivo.
Here, we have demonstrated that seminal vesicle protein
secretion 2 (SVS2), a 40-kDa basic protein and a major
component of the copulatory plug, enters the uterus and
interacts with ejaculated sperm heads after copulation.
The SVS2-binding region of sperm changes from the
postacrosomal region to the equatorial segment while the
sperm migrates through the uterus and finally disappears
in the oviduct. Furthermore, SVS2 reduces the fertility of
epididymal sperm. The sperm treated with SVS2 decreases
the percentage of fertilized oocytes from 60% to 10%. The
capacitation state was assessed by protein tyrosine
phosphorylation and the comprehensiveness of the acrosome
reaction. In results, SVS2 functioned to maintain sperm in
the uncapacitated state and to reverse capacitated sperm
to the uncapacitated state. We found that the fertility of
ejaculated sperm is associated with SVS2 distribution in
the female reproductive tract. These results indicate that
SVS2 functions as a decapacitation factor for mouse sperm.
Key words:
Female Reproductive Tract •
Male Reproductive Tract •
Fertilization •
Seminal vesicles •
Sperm capacitation
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