Xu X-Z Shawn, Sternberg Paul W
Howard Hughes Medical Institute and Division of Biology, California Institute of Technology, Pasadena, CA 91125 USA.
Cell. 2003 Aug 8;114(3):285-97. doi: 10.1016/s0092-8674(03)00565-8.
Fertilization, a critical step in animal reproduction, is triggered by a series of specialized sperm-egg interactions. However, the molecular mechanisms underlying fertilization are not well understood. Here, we identify a sperm-enriched C. elegans TRPC homolog, TRP-3. Mutations in trp-3 lead to sterility in both hermaphrodites and males due to a defect in their sperm. trp-3 mutant sperm are motile, but fail to fertilize oocytes after gamete contact. TRP-3 is initially localized in intracellular vesicles, and then translocates to the plasma membrane during sperm activation. This translocation coincides with a marked increase in store-operated calcium entry, providing an in vivo mechanism for the regulation of TRP-3 activity. As C. elegans oocytes lack egg coats, our data suggest that some TRPC family channels might function to mediate calcium influx during sperm-egg plasma membrane interactions leading to fertilization.
受精是动物繁殖过程中的关键步骤，由一系列特殊的精卵相互作用引发。然而，受精背后的分子机制尚未得到充分理解。在此，我们鉴定出一种在精子中高度富集的秀丽隐杆线虫TRPC同源物TRP-3。trp-3基因的突变会导致雌雄同体和雄性线虫均不育，原因是其精子存在缺陷。trp-3突变体精子具有运动能力，但在配子接触后无法使卵母细胞受精。TRP-3最初定位于细胞内囊泡，然后在精子激活过程中转位至质膜。这种转位与储存式钙内流的显著增加相吻合，为TRP-3活性的调节提供了一种体内机制。由于秀丽隐杆线虫的卵母细胞没有卵膜，我们的数据表明，一些TRPC家族通道可能在精卵质膜相互作用导致受精的过程中发挥作用，介导钙内流。
