title: Seminal vesicle proteins SVS3 and SVS4 facilitate SVS2 effect on sperm capacitation.
abstract: Mammalian spermatozoa acquire their fertilizing ability in the female reproductive tract (sperm capacitation). On the other hand, seminal vesicle secretion, which is a major component of seminal plasma, inhibits the initiation of sperm capacitation (capacitation inhibition) and reduces the fertility of the capacitated spermatozoa (decapacitation). There are seven major proteins involved in murine seminal vesicle secretion (SVS1-7), and we have previously shown that SVS2 acts as both a capacitation inhibitor and a decapacitation factor, and is indispensable for in vivo fertilization. However, the effects of SVSs other than SVS2 on the sperm have not been elucidated. Since mouse Svs2-Svs6 genes evolved by gene duplication belong to the same gene family, it is possible that SVSs other than SVS2 also have some effects on sperm capacitation. In this study, we examined the effects of SVS3 and SVS4 on sperm capacitation. Our results showed that both SVS3 and SVS4 are able to bind to spermatozoa, but SVS3 alone showed no effects on sperm capacitation. On the other hand, SVS4 acted as a capacitation inhibitor, although it did not show decapacitation abilities. Interestingly, SVS3 showed an affinity for SVS2 and it facilitated the effects of SVS2. Interaction of SVS2 and spermatozoa is mediated by the ganglioside GM1 in the sperm membrane; however, both SVS3 and SVS4 had weaker affinities for GM1 than SVS2. Therefore, we suggest that separate processes may cause capacitation inhibition and decapacitation, and SVS3 and SVS4 act on sperm capacitation cooperatively with SVS2.
authors.affiliation: Misaki Marine Biological StationSchool of Science, The University of Tokyo, Miura, Kanagawa, Japan.
authors.forename: Naoya
authors.initials: N
authors.lastname: Araki
authors.affiliation: Department of AgricultureMeiji University, Kawasaki, Kanagawa, Japan Department of Reproductive BiologyNational Center for Child Health and Development, Setagaya, Tokyo, Japan.
authors.forename: Natsuko
authors.initials: N
authors.lastname: Kawano
authors.affiliation: Department of AgricultureMeiji University, Kawasaki, Kanagawa, Japan Department of Reproductive BiologyNational Center for Child Health and Development, Setagaya, Tokyo, Japan.
authors.forename: Woojin
authors.initials: W
authors.lastname: Kang
authors.affiliation: Department of Reproductive BiologyNational Center for Child Health and Development, Setagaya, Tokyo, Japan.
authors.forename: Kenji
authors.initials: K
authors.lastname: Miyado
authors.affiliation: Biomedical Engineering CenterToin University of Yokohama, Yokohama, Kanagawa, Japan.
authors.forename: Kaoru
authors.initials: K
authors.lastname: Yoshida
authors.affiliation: Misaki Marine Biological StationSchool of Science, The University of Tokyo, Miura, Kanagawa, Japan Center for Marine BiologyThe University of Tokyo, Miura, Kanagawa, Japan yoshida@mmbs.s.u-tokyo.ac.jp.
authors.forename: Manabu
authors.initials: M
authors.lastname: Yoshida
mesh_terms: D000818:Animals; D005260:Female; D005298:Fertility / Q000502:physiology*; D008297:Male; D051379:Mice; D029607:Seminal Vesicle Secretory Proteins / Q000378:metabolism*; D013075:Sperm Capacitation / Q000502:physiology*; D013094:Spermatozoa / Q000378:metabolism
chemical_list: C520624:SVS2 protein, mouse; C573954:SVS4 protein, mouse; D029607:Seminal Vesicle Secretory Proteins