CACN-1/Cactin interacts genetically with MIG-2 GTPase signaling to control distal tip cell migration in C. elegans.
CACN-1/Cactin interacts genetically with MIG-2 GTPase signaling to control distal tip cell migration in C. elegans.
复制标题
CACN-1/Cactin 与 MIG-2 GTPase 信号传导发生遗传相互作用，以控制秀丽隐杆线虫的远端细胞迁移。
DOI：
10.1016/j.ydbio.2010.02.025
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发表时间：
2010
影响因子：
2.7
通讯作者：
Cram,ErinJ
中科院分区：
文献类型：
--
作者：
Tannoury,Hiba;Rodriguez,Varenka;Kovacevic,Ismar;Ibourk,Mouna;Lee,Myeongwoo;Cram,ErinJ
这两个专业的C。线虫远端细胞（DTC）为研究发育调节的细胞迁移提供了体内模型系统。我们在全基因组RNAi筛选DTC迁移调节因子中鉴定了cacn-1/cactin，这是一种保守的新型细胞迁移调节因子。RNAi耗竭实验和亚纯型等位基因cacn-1（tm 3126）的分析表明，CACN-1是需要在DTC迁移过程中适当的寻路和停止DTC迁移在幼虫形态发生结束。DTC中CACN-1的强表达以及来自细胞特异性RNAi耗竭实验的数据表明，需要CACN-1细胞自主地控制DTC迁移。重要的是，与Rac GTP酶激活剂和效应物的遗传相互作用数据表明，CACN-1特异性抑制mig-2/Rac通路，并与ced-10/Rac平行，控制DTC寻路。
The two specialized C. elegans distal tip cells (DTCs) provide an in vivo model system for the study of developmentally regulated cell migration. We identified cacn-1/cactin, a well-conserved, novel regulator of cell migration in a genome-wide RNAi screen for regulators of DTC migration. RNAi depletion experiments and analysis of the hypomorphic allele cacn-1(tm3126) indicate that CACN-1 is required during DTC migration for proper pathfinding and for cessation of DTC migration at the end of larval morphogenesis. Strong expression of CACN-1 in the DTCs, and data from cell-specific RNAi depletion experiments, suggest that CACN-1 is required cell-autonomously to control DTC migration. Importantly, genetic interaction data with Rac GTPase activators and effectors suggest that CACN-1 acts specifically to inhibit the mig-2/Rac pathway, and in parallel to ced-10/Rac, to control DTC pathfinding.