CACN-1/Cactin interacts genetically with MIG-2 GTPase signaling to control distal tip cell migration in C. elegans.
Hiba Tannoury, Varenka Rodriguez, Ismar Kovacevic, Mouna Ibourk, Myeongwoo Lee, Erin J Cram
Author Information
Hiba Tannoury: Department of Biology, Northeastern University, 360 Huntington Ave, 134 Mugar Hall, Boston, MA 02115, USA.
中文译文
English
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.
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R01 GM085077/NIGMS NIH HHS
R01 GM085077-02/NIGMS NIH HHS
GM085077/NIGMS NIH HHS
Animals
Caenorhabditis elegans
Caenorhabditis elegans Proteins
Carrier Proteins
Cell Movement
Drosophila Proteins
Gonads
rac GTP-Binding Proteins
Caenorhabditis elegans Proteins
Carrier Proteins
Drosophila Proteins
cactin protein, Drosophila
Mig-2 protein, C elegans
rac GTP-Binding Proteins