Role and regulation of PI3K in sperm capacitation and the acrosome reaction
Role and regulation of PI3K in sperm capacitation and the acrosome reaction
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DOI：
10.1016/j.mce.2009.06.009
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发表时间：
2010-01-27
影响因子：
4.1
通讯作者：
Etkovitz, Nir
中科院分区：
文献类型：
--
作者：
Breitbart, Haim;Rotman, Tali;Etkovitz, Nir
哺乳动物精子在雌性生殖道中经历几种信号和生化转化，统称为获能。获能的精子与卵细胞结合，在那里它经历顶体反应（AR），这是一个使它能够穿透卵细胞并使其受精的过程。肌动蛋白聚合发生在精子获能和解聚之前的AR。本文综述了PI3K在精子获能和顶体反应中的作用及其调控。我们声称PI3K被蛋白激酶A激活，并被蛋白激酶C抑制。在获能时间期间仅观察到PI3K的部分活化，然而在孵育结束时，观察到完全活化。获能过程中的肌动蛋白聚合是独立的PI3K活性，表明该酶不参与精子获能。然而，在获能结束时PI3 K的完全激活表明它可能介导AR，正如确实发现的那样。（C）2009 Elsevier爱尔兰有限公司保留所有权利。
Mammalian spermatozoa undergo several signaling and biochemical transformations in the female genital tract, collectively called capacitation. The capacitated spermatozoon binds to the egg zona pellucida, where it undergoes the acrosome reaction (AR), a process enabling it to penetrate and fertilize the egg. Actin polymerization occurs in sperm capacitation and depolymerization prior to the AR. In this review we describe the possible role and regulation of PI3K in sperm capacitation and the acrosome reaction. We claim that PI3K is activated by protein kinase A and suppressed by protein kinase C. Only partial activation of PI3K is seen during the capacitation time, however towards the end of incubation, full activation is observed. Actin polymerization during capacitation is independent on PI3K activity, suggesting that the enzyme is not involved in sperm capacitation. However, the full activation of PI3K towards the end of the capacitation suggests that it might mediate the AR, as indeed was found. (C) 2009 Elsevier Ireland Ltd. All rights reserved.