Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
FEBS Lett. 2010 Mar 5;584(5):1041-6. doi: 10.1016/j.febslet.2010.02.005. Epub 2010 Feb 9.
Here we show a unique example of male infertility conferred by a gene knockout of the sperm-specific, pH-dependent SLO3 potassium channel. In striking contrast to wild-type sperm which undergo membrane hyperpolarization during capacitation, we found that SLO3 mutant sperm undergo membrane depolarization. Several defects in SLO3 mutant sperm are evident under capacitating conditions, including impaired motility, a bent "hairpin" shape, and failure to undergo the acrosome reaction (AR). The failure of AR is rescued by valinomycin which hyperpolarizes mutant sperm. Thus SLO3 is the principal potassium channel responsible for capacitation-induced hyperpolarization, and membrane hyperpolarization is crucial to the AR.
在这里，我们展示了一个独特的男性不育症的例子，其由精子特异性、pH 依赖性 SLO3 钾通道的基因敲除引起。与在获能过程中经历膜超极化的野生型精子形成鲜明对比的是，我们发现 SLO3 突变体精子经历膜去极化。在获能条件下，SLO3 突变体精子的几个缺陷是明显的，包括运动能力受损、弯曲的“发夹”形状以及无法发生顶体反应 (AR)。用缬氨霉素（valinomycin）使突变体精子超极化可以挽救 AR 的失败。因此，SLO3 是负责获能诱导超极化的主要钾通道，而膜超极化对于 AR 至关重要。
