C. elegans POP-1/TCF functions in a canonical Wnt pathway that controls cell migration and in a noncanonical Wnt pathway that controls cell polarity.
C. elegans POP-1/TCF functions in a canonical Wnt pathway that controls cell migration and in a noncanonical Wnt pathway that controls cell polarity.
复制标题
作者：
Michael A. Herman
在秀丽隐杆线虫中，Wnt信号通路在控制细胞极性和细胞迁移中起重要作用。在胚胎中，一种新的Wnt通路通过（β）-连环蛋白同源物WRM-1发挥作用，下调EMS卵裂球后部子代中POP-1/Tcf的水平。POP-1的水平也较低，在许多前后不对称的细胞分裂发育过程中的后女儿。我发现这是尾部一对胚后母细胞的情况。在野生型动物中，POP-1的水平在两个T细胞TL和TR的后子代中较低。此外，在lin-44/Wnt突变体中，其中T细胞分裂的极性经常逆转，POP-1的水平在T细胞的前子代中经常较低。我已经使用了一种新的RNA介导的干扰技术，专门干扰pop-1合子功能，并已确定pop-1是野生型T细胞极性所必需的。令人惊讶的是，这三个C。线虫（β）-连环蛋白同源物似乎与POP-1一起起作用以控制T细胞极性。EGL-20/Wnt的Wnt信号通过调节Hox基因mAb-5的表达来控制QL成神经细胞后代的迁移。干扰pop-1合子功能导致QL后代迁移缺陷，其模仿egl-20/Wnt突变体中的缺陷并阻断mAb-5的表达。这表明POP-1在经典Wnt途径中起作用以控制QL后代迁移，并且在新Wnt途径中起作用以控制EMS和T细胞极性。
In Caenorhabditis elegans, Wnt signaling pathways are important in controlling cell polarity and cell migrations. In the embryo, a novel Wnt pathway functions through a (beta)-catenin homolog, WRM-1, to downregulate the levels of POP-1/Tcf in the posterior daughter of the EMS blastomere. The level of POP-1 is also lower in the posterior daughters of many anteroposterior asymmetric cell divisions during development. I have found that this is the case for of a pair of postembryonic blast cells in the tail. In wild-type animals, the level of POP-1 is lower in the posterior daughters of the two T cells, TL and TR. Furthermore, in lin-44/Wnt mutants, in which the polarities of the T cell divisions are frequently reversed, the level of POP-1 is frequently lower in the anterior daughters of the T cells. I have used a novel RNA-mediated interference technique to interfere specifically with pop-1 zygotic function and have determined that pop-1 is required for wild-type T cell polarity. Surprisingly, none of the three C. elegans (beta)-catenin homologs appeared to function with POP-1 to control T cell polarity. Wnt signaling by EGL-20/Wnt controls the migration of the descendants of the QL neuroblast by regulating the expression the Hox gene mab-5. Interfering with pop-1 zygotic function caused defects in the migration of the QL descendants that mimicked the defects in egl-20/Wnt mutants and blocked the expression of mab-5. This suggests that POP-1 functions in the canonical Wnt pathway to control QL descendant migration and in novel Wnt pathways to control EMS and T cell polarities.