Deletion of Eqtn in mice reduces male fertility and sperm-egg adhesion
Deletion of Eqtn in mice reduces male fertility and sperm-egg adhesion
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DOI：
10.1530/rep-18-0394
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发表时间：
2018-12-01
期刊：
影响因子：
3.8
通讯作者：
Toshimori, Kiyotaka
中科院分区：
文献类型：
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作者：
Ito, Chizuru;Yamatoya, Kenji;Toshimori, Kiyotaka
许多精子蛋白参与了从配子粘附到融合的过程，但其潜在机制尚不清楚。在这里，我们建立了小鼠突变体，即equatorin敲除（Eqtn - ko, Eqtn(-/-)）小鼠模型，发现Eqtn - ko雄性的生育能力和精子-卵子粘连降低，而Eqtn - ko雌性具有生育能力。精子形态和运动正常。通过Eqtn（-/-）与Eqtn(+/+)- tg （Acr-Egfp）小鼠杂交产生的顶体报告基因Eqtn(-/-)- tg （Acr-Egfp）精子到达WT雌性的输卵管壶腹，穿透卵透明带。然而，与WT雌性交配的Eqtn（-/-）雄性小鼠的生育能力和附着在无带卵母细胞上的精子数量均显著降低。精子IZUMO1和卵子CD9在与WT卵子受精的Eqtn（-/-）精子中表现正常。顶体反应期间，另一种顶体蛋白SPESP1在Eqtn（-/-）精子中表现异常。EQTN/ Spesp1 -双KO雄性（EQTN/ Spesp1(-/-)）与EQTN（-/-）雄性相比，EQTN/ Spesp1（-/-）缺失的雄性生育能力受损更为严重。为挽救Eqtn（-/-）雄性而产生的Eqtn(-/-)- tg （Eqtn）雄性恢复了下降的生育能力。
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.