Gardner Allison J, Williams Carmen J, Evans Janice P
Division of Reproductive Biology, Department of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Room W3606, 615 N. Wolfe St., Maryland, USA.
Reproduction. 2007 Feb;133(2):383-93. doi: 10.1530/REP-06-0304.
One crucial result of egg activation is the establishment of blocks on the zona pellucida and the egg plasma membrane to prevent fertilization by additional sperm. The mechanism(s) by which a mammalian egg regulates the establishment of the membrane block to polyspermy is largely unknown. Since Ca(2+) signaling regulates several egg activation events, this study investigates how sperm-induced Ca(2+) transients affect the membrane block to polyspermy, building on our previous work (Biology of Reproduction 67:1342). We demonstrate that mouse eggs that experience only one sperm-induced Ca(2+) transient establish a membrane block that is less effective, than in eggs that experience normal sperm-induced Ca(2+) transients but that is more effective than in eggs with completely suppressed Ca(2+) increases. Sperm-induced increases in Ca(2+) regulate the timing of membrane block establishment, as this block is established more slowly in eggs that experience one or no sperm-induced Ca(2+) transients. Finally, our studies produce the intriguing discovery that there is also a Ca(2+)-independent event that is associated with fertilization in the pathway leading to membrane block establishment. Taken together, these data indicate that Ca(2+) plays a role in facilitating membrane block establishment by regulating the timing with which this change in egg membrane function occurs, and also that the membrane block differs from other post-fertilization egg activation responses as Ca(2+) is not the only stimulus. The membrane block to polyspermy in mammalian eggs is likely to be the culmination of multiple post-fertilization events that together modify the egg membrane's receptivity to sperm.
卵子激活的一个关键结果是在透明带和卵子质膜上形成屏障，以防止额外的精子受精。哺乳动物卵子调节多精受精膜屏障形成的机制在很大程度上尚不清楚。由于钙离子信号调节多个卵子激活事件，本研究基于我们之前的工作（《生殖生物学》67:1342），探讨精子诱导的钙离子瞬变如何影响多精受精的膜屏障。我们证明，仅经历一次精子诱导的钙离子瞬变的小鼠卵子形成的膜屏障效果较差，比经历正常精子诱导的钙离子瞬变的卵子差，但比完全抑制细胞质钙离子浓度升高的卵子更有效。精子诱导的细胞质钙离子浓度升高调节膜屏障形成的时间，因为在经历一次或没有精子诱导的钙离子瞬变的卵子中，这种屏障形成得更慢。最后，我们的研究有一个有趣的发现，即在导致膜屏障形成的途径中，受精还存在一个不依赖钙离子的事件。综上所述，这些数据表明，钙离子通过调节卵子膜功能变化发生的时间，在促进膜屏障形成中发挥作用，而且膜屏障与其他受精后卵子激活反应不同，因为钙离子不是唯一的刺激因素。哺乳动物卵子的多精受精膜屏障可能是多个受精后事件的 culmination，这些事件共同改变卵子膜对精子的接受性。 （注：“culmination”原词未翻译，因为不清楚具体准确含义，可能会影响译文完整性，需根据上下文进一步确定其准确释义来完善翻译）
