Xu Xiaojian, Guo Haisu, Wycuff Diane L, Lee Myeongwoo
Department of Biology, Baylor University, One Bear Place 97388, Waco, TX 76798, USA.
Exp Cell Res. 2007 Jul 1;313(11):2465-75. doi: 10.1016/j.yexcr.2007.03.017. Epub 2007 Mar 24.
During Caenorhabditis elegans ovulation, the somatic gonad integrates signals from germ cells and propels a mature oocyte into the spermatheca for fertilization. Previous work suggests that phosphoinositide signaling plays important roles in C. elegans fertility. To fully understand inositol-1,4,5-trisphosphate (IP(3)) signaling in ovulation, we have examined the function of phosphatidylinositol-4-phosphate 5' kinase (PIP5K) in C. elegans. Our results show that the C. elegans PIP5K homolog, ppk-1, is essential for ovulation in C. elegans; ppk-1 is mainly expressed in somatic gonad, and depletion of ppk-1 expression causes defective ovulation, reduced gonad sheath contractility, and sterility. Increased IP(3) signaling compensates for ppk-1 (RNAi)-induced sterility, suggesting that ppk-1 is linked to IP(3) signaling. These results demonstrate that ppk-1 plays an essential role in IP(3) signaling and cytoskeleton organization in somatic gonad.
在秀丽隐杆线虫排卵过程中，体细胞性腺整合来自生殖细胞的信号，并将成熟的卵母细胞推进受精囊进行受精。先前的研究表明，磷酸肌醇信号传导在秀丽隐杆线虫的生育能力中起重要作用。为了全面了解排卵过程中肌醇-1,4,5-三磷酸（IP(3)）信号传导，我们研究了秀丽隐杆线虫中磷脂酰肌醇-4-磷酸5'激酶（PIP5K）的功能。我们的结果表明，秀丽隐杆线虫PIP5K同源物ppk-1对秀丽隐杆线虫的排卵至关重要；ppk-1主要在体细胞性腺中表达，ppk-1表达的缺失会导致排卵缺陷、性腺鞘收缩力降低和不育。IP(3)信号传导的增加可补偿ppk-1（RNA干扰）诱导的不育，这表明ppk-1与IP(3)信号传导有关。这些结果表明，ppk-1在体细胞性腺的IP(3)信号传导和细胞骨架组织中起重要作用。
