Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Dev Biol. 2010 May 1;341(1):176-85. doi: 10.1016/j.ydbio.2010.02.025. Epub 2010 Feb 25.

CACN-1/Cactin interacts genetically with MIG-2 GTPase signaling to control distal tip cell migration in C. elegans.

Author information

  • 1Department of Biology, Northeastern University, 360 Huntington Ave, 134 Mugar Hall, Boston, MA 02115, USA.

Erratum in

  • Dev Biol. 2010 Aug 15;344(2):e1.

Abstract

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.

Copyright 2010 Elsevier Inc. All rights reserved.

PMID:
20188721
[PubMed - indexed for MEDLINE]
PMCID:
PMC2854247
Free PMC Article

Images from this publication.See all images (6)Free text

Fig. 1
Fig. 2
Fig. 3
Fig. 4
Fig. 5
Fig 6
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk