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Resources » Paper

Rocheleau, Simon K. et al. (2011) International Worm Meeting "The roles of rhgf-2/Rho GEF and fhod-1/formin in regulating the actin cytoskeleton during embryonic elongation."

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  • Comments on Rocheleau, Simon K. et al. (2011) International Worm Meeting "The roles of rhgf-2/Rho GEF and fhod-1/formin in regulating the actin cytoskeleton during embryonic elongation." (0)

  • Overview

    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00038650

    Rocheleau, Simon K., Vanneste, Christopher A., Raharjo, Eko, Steven, Robert, Pruyne, David, & Mains, Paul E. (2011). The roles of rhgf-2/Rho GEF and fhod-1/formin in regulating the actin cytoskeleton during embryonic elongation presented in International Worm Meeting. Unpublished information; cite only with author permission.

    Embryonic elongation, which transforms the roughly spherical embryo into a long, thin vermiform larva, is mediated in part by a smooth muscle-like contraction of an actin/myosin network in the epidermal cells. Here we describe two new players that regulate this process. Previous work has shown that contractile force is generated by two redundant pathways that activate non-muscle myosin. Contraction is triggered by the phosphorylation of MLC-4, which activates the non-muscle myosins NMY-1/NMY-2. This is counteracted by MLC-4 dephosphorylation by MEL-11/myosin phosphatase. One of the two contractile pathways involves the small GTPase RHO-1, which activates LET-502/Rho-binding kinase, which in turn inhibits the MEL-11 brake to contraction. A second, parallel pathway involves FEM-2/protein phosphatase 2c. In a suppressor screen of mel-11, we isolated an allele of a Rho GEF (guanine exchange factor), rhgf-2. As expected, rhgf-2 genetically behaves as an upstream activator of the let-502/Rho-binding kinase branch of the elongation pathway and appears to function in parallel to fem-2. RHGF-2 binds to and acts as a GEF for RHO-1 (See abstract by Tran et al.). Even though circumferential actin filaments are present in all epidermal cells, most of the contractile force is generated by the lateral (seam) cells. The lateral cell microfilaments are qualitatively different than those in their dorsal and ventral neighbours in that they are found further from the apical surface. We have identified a actin nucleator in the formin family that may be in part responsible for these differences. FHOD-1 (formin homology domain) is expressed only in the lateral epidermal cells and mutations cause actin defects only in those cells. Curiously, genetic results indicate that fhod-1 acts downstream of let-502 and in parallel to fem-2, implying that the two pathways may act on different sets of microfilaments.

    Affiliations:
    - Department of Cell and Developmental Biology, SUNY Upstate Medical University, Syracuse, NY
    - Dept Biochem & Molec Biol, Univ Calgary, Calgary, AB, Canada
    - Department of Biological Sciences, University of Toledo, Toledo, OH


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