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  • Author: Yutaka Tamura x
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Chizuru Ito, Kenji Yamatoya, Keiichi Yoshida, Lisa Fujimura, Hajime Sugiyama, Akiko Suganami, Yutaka Tamura, Masahiko Hatano, Kenji Miyado and Kiyotaka Toshimori

A number of sperm proteins are involved in the processes from gamete adhesion to fusion, but the underlying mechanism is still unclear. Here, we established a mouse mutant, the EQUATORIN-knockout (EQTN-KO, Eqtn / ) mouse model and found that the EQTN-KO males have reduced fertility and sperm–egg adhesion, while the EQTN-KO females are fertile. Eqtn / sperm were normal in morphology and motility. Eqtn / -Tg (Acr-Egfp) sperm, which were produced as the acrosome reporter by crossing Eqtn / with Eqtn +/+-Tg(Acr-Egfp) mice, traveled to the oviduct ampulla and penetrated the egg zona pellucida of WT females. However, Eqtn / males mated with WT females showed significant reduction in both fertility and the number of sperm attached to the zona-free oocyte. Sperm IZUMO1 and egg CD9 behaved normally in Eqtn / sperm when they were fertilized with WT egg. Another acrosomal protein, SPESP1, behaved aberrantly in Eqtn / sperm during the acrosome reaction. The fertility impairment of EQTN/SPESP1-double KO males lacking Eqtn and Spesp1 (Eqtn/Spesp1 / ) was more severe compared with that of Eqtn / males. Eqtn / -Tg (Eqtn) males, which were generated to rescue Eqtn / males, restored the reduced fertility.