Reduced fertility of mouse epididymal sperm lacking Prss21/Tesp5 is rescued by sperm exposure to uterine microenvironment
Reduced fertility of mouse epididymal sperm lacking Prss21/Tesp5 is rescued by sperm exposure to uterine microenvironment
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DOI：
10.1111/j.1365-2443.2008.01222.x
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发表时间：
2008-10-01
期刊：
影响因子：
2.1
通讯作者：
Baba, Tadashi
中科院分区：
文献类型：
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作者：
Yamashita, Misuzu;Honda, Arata;Baba, Tadashi
虽然顶体反应和精子穿透卵透明膜（ZP）是哺乳动物受精的必要条件，但其分子机制仍存在争议。我们以前已经确定了丝氨酸蛋白酶Tesp 5相同的Prss 21在小鼠精子表面作为一个候选酶参与精子穿透ZP。在这里，我们表明，尽管正常生育的雄性小鼠缺乏Prss 21/Tesp 5，附睾精子穿透ZP只有在一个非常低的速度在体外，大概是由于能力降低结合ZP和进行ZP诱导的顶体反应。Prss 21-null精子在体外与卵子融合的能力也严重受损。有趣的是，Prss 21无效的附睾精子的生育力降低，通过将精子暴露于子宫微环境和通过用子宫液体外处理精子来挽救。这些数据表明精子通过子宫运输的生理重要性。
Although the acrosome reaction and subsequent penetration of sperm through the egg zona pellucida (ZP) are essential for mammalian fertilization, the molecular mechanism is still controversial. We have previously identified serine protease Tesp5 identical to Prss21 on the mouse sperm surface as a candidate enzyme involved in sperm penetration through the ZP. Here we show that despite normal fertility of male mice lacking Prss21/Tesp5, the epididymal sperm penetrates the ZP only at a very low rate in vitro, presumably owing to the reduced ability to bind the ZP and undergo the ZP-induced acrosome reaction. The ability of Prss21-null sperm to fuse with the egg in vitro was also impaired severely. Intriguingly, the reduced fertility of Prss21-null epididymal sperm was rescued by exposure of the sperm to the uterine microenvironment and by in vitro treatment of the sperm with uterine fluids. These data suggest the physiological importance of sperm transport through the uterus.