Nakaya M, Fukui A, Izumi Y, Akimoto K, Asashima M, Ohno S
Department of Molecular Biology, Yokohama City University School of Medicine, Yokohama 236-0004, Japan.
Development. 2000 Dec;127(23):5021-31. doi: 10.1242/dev.127.23.5021.
The asymmetric distribution of cellular components is an important clue for understanding cell fate decision during embryonic patterning and cell functioning after differentiation. In C. elegans embryos, PAR-3 and aPKC form a complex that colocalizes to the anterior periphery of the one-cell embryo, and are indispensable for anterior-posterior polarity that is formed prior to asymmetric cell division. In mammals, ASIP (PAR-3 homologue) and aPKCgamma form a complex and colocalize to the epithelial tight junctions, which play critical roles in epithelial cell polarity. Although the mechanism by which PAR-3/ASIP and aPKC regulate cell polarization remains to be clarified, evolutionary conservation of the PAR-3/ASIP-aPKC complex suggests their general role in cell polarity organization. Here, we show the presence of the protein complex in Xenopus laevis. In epithelial cells, XASIP and XaPKC colocalize to the cell-cell contact region. To our surprise, they also colocalize to the animal hemisphere of mature oocytes, whereas they localize uniformly in immature oocytes. Moreover, hormonal stimulation of immature oocytes results in a change in the distribution of XaPKC 2-3 hours after the completion of germinal vesicle breakdown, which requires the kinase activity of aPKC. These results suggest that meiotic maturation induces the animal-vegetal asymmetry of aPKC.
细胞成分的不对称分布是理解胚胎模式形成过程中细胞命运决定以及分化后细胞功能的重要线索。在秀丽隐杆线虫胚胎中,PAR-3和非典型蛋白激酶C(aPKC)形成一个复合物,该复合物共定位于单细胞胚胎的前周边,并且对于在不对称细胞分裂之前形成的前后极性是不可或缺的。在哺乳动物中,ASIP(PAR-3同源物)和aPKCγ形成一个复合物并共定位于上皮紧密连接,上皮紧密连接在上皮细胞极性中起关键作用。尽管PAR-3/ASIP和aPKC调节细胞极化的机制仍有待阐明,但PAR-3/ASIP-aPKC复合物的进化保守性表明它们在细胞极性组织中具有普遍作用。在这里,我们展示了非洲爪蟾中存在该蛋白复合物。在上皮细胞中,XASIP和XaPKC共定位于细胞-细胞接触区域。令我们惊讶的是,它们还共定位于成熟卵母细胞的动物半球,而在未成熟卵母细胞中它们均匀分布。此外,对未成熟卵母细胞的激素刺激在生发泡破裂完成后2 - 3小时导致XaPKC分布发生变化,这需要aPKC的激酶活性。这些结果表明减数分裂成熟诱导了aPKC的动物-植物不对称性。