Department of Biochemistry, Chonbuk National University Medical School, Jeonju 561-180, Korea.
Sci Signal. 2011 May 17;4(173):ra31. doi: 10.1126/scisignal.2001595.
Progesterone-induced calcium ion (Ca2+) signals in the neck region of sperm play a pivotal role in promoting sperm motility. Here, we show that a long-lasting Ca2+ signal required for sperm motility in response to progesterone depends on their pH-dependent fusion with prostasomes, which are small vesicles secreted by the prostate. We found that prostasome fusion led to the transfer of progesterone receptors, cyclic adenosine diphosphoribose (cADPR)-synthesizing enzymes, ryanodine receptors (RyRs), and other Ca2+ signaling tools from prostasomes to the sperm neck. Progesterone-induced sperm motility relied on cADPR-mediated Ca2+ mobilization through RyR located on acidic Ca2+ stores, followed by Ca2+ entry through store-operated channels. Treatment of prostasome-fused sperm with a cADPR antagonist or fusion with prostasomes in which type 2 RyR was depleted resulted in low fertilization rates, reduced sperm motility, or both. Thus, we conclude that sperm motility depends on the acquisition of Ca2+ signaling tools from prostasomes.
孕激素诱导的精子颈部钙离子（Ca2+）信号在促进精子运动中起着关键作用。在这里，我们表明，对孕激素反应所需的持续时间较长的 Ca2+信号取决于它们与前列腺小体的 pH 依赖性融合，前列腺小体是前列腺分泌的小囊泡。我们发现，前列腺体融合导致孕激素受体、环腺苷二磷酸核糖（cADPR）合成酶、ryanodine 受体（RyR）和其他 Ca2+信号转导工具从前列腺体转移到精子颈部。孕激素诱导的精子运动依赖于 cADPR 介导的通过位于酸性 Ca2+储存库上的 RyR 的 Ca2+动员，随后通过储存操作通道进行 Ca2+内流。用 cADPR 拮抗剂处理融合前列腺体的精子或用耗尽 2 型 RyR 的前列腺体融合，会导致受精率降低、精子运动能力降低或两者兼有。因此，我们得出结论，精子运动依赖于从前列腺小体获得 Ca2+信号转导工具。
