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Ganglioside GM1 Mediates Decapacitation Effects of SVS2 on Murine Spermatozoa¹

Misaki Marine Biological Station,⁴ Graduate School of Science, University of Tokyo, Kanagawa 238-0225, Japan Biomedical Engineering Center,⁵ Toin University of Yokohama, Yokohama 225-8502, Japan Division of Male Infertility,⁶ Center for Infertility and IVF, International University of Health and Welfare, Tochigi 329-2763, Japan

ABSTRACT

Prior to fertilization, mammalian spermatozoa need to acquire fertilizing ability (capacitation) in the female reproductive tract. On the other hand, capacitated spermatozoa reversibly lose their capacitated state when treated with seminal plasma (decapacitation). Previously, we demonstrated that a mouse seminal plasma protein, SVS2, is a decapacitation factor and regulates sperm fertilizing ability in vivo. Here, we examined the mechanisms of regulation of fertilizing ability by SVS2. Capacitation appears to be mediated by dynamic changes in lipid rafts since release of the cholesterol components of lipid rafts in the sperm plasma membrane is indispensable for capacitation. When the ejaculated spermatozoa were stained with a cholera toxin subunit B (CTB) that preferably interacts with ganglioside GM1, another member of the lipid rafts, the staining pattern of the sperm was the same as the binding pattern of SVS2. Interestingly, SVS2 and CTB competitively bound to the sperm surface with each other, suggesting that the binding targets of both molecules are the same, that is, GM1. Molecular interaction studies by the overlay assay and the quartz crystal microbalance analysis revealed that SVS2 selectively interacts with GM1 rather than with other gangliosides. Furthermore, external addition of GM1 nullified SVS2-induced sperm decapacitation. Thus, ganglioside GM1 is a receptor of SVS2 and plays a crucial role in capacitation in vivo.

decapacitation factor, female reproductive tract, fertilization, ganglioside GM1, mouse, seminal vesicles, signal transduction, sperm, sperm capacitation, SVS2

¹Supported in part by Grants-in-Aid for Scientific Research from MEXT and JSPS (KAKENHI) (#19370028, #19037012, and #19045008) to M.Y.

Correspondence: ²Manabu Yoshida, Misaki Marine Biological Station, Graduate School of Science University of Tokyo, Miura, Kanagawa 238-0225, Japan. FAX: 81 46 881 7944; e-mail: yoshida{at}mmbs.s.u-tokyo.ac.jp

³Current address: Life Sciences and Bioengineering, Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba 305-8572, Japan.