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Resources » Paper

Viveiros, Ryan et al. (2013) International Worm Meeting "UNC-54 and Y54E5B.2 work in concert to inhibit ectopic membrane extensions away from the nerve cord in C. elegans body wall muscle."

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  • Comments on Viveiros, Ryan et al. (2013) International Worm Meeting "UNC-54 and Y54E5B.2 work in concert to inhibit ectopic membrane extensions away from the nerve cord in C. elegans body wall muscle." (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00042773

    Viveiros, Ryan, Schnabel, Ralf, Barstead, Robert, & Moerman, Donald (2013). UNC-54 and Y54E5B.2 work in concert to inhibit ectopic membrane extensions away from the nerve cord in C. elegans body wall muscle presented in International Worm Meeting. Unpublished information; cite only with author permission.

    Adult C. elegans have 95 body wall muscle cells arranged in 4 quadrants, each consisting of two longitudinal rows of cells running along the length of the animal. The two ventral quadrants flank the ventral nerve and the two dorsal quadrants flank the dorsal nerve cord. These muscle cells, both those proximal and those distal to their adjacent nerve cord, extend specialized membrane extensions called muscle arms to establish contact with the nerve cord. These are the only membrane projections extended by adult body wall muscle cells. In a screen for mutants with muscle defects, we have identified a temperature sensitive strain, GE6583, which exhibits ectopic membrane extensions away from the nerve cords at the non-permissive temperature. These projections can be quite extensive. We have observed processes originating from a ventral or dorsal cell extending across the animal to make contact with a cell in a quadrant on the opposite side of the animal. Mapping and sequencing studies of the strain reveal two tightly linked candidate genes, unc-54(t3197), the C. elegans myosin heavy chain B homologue, and Y54E5B.2(t3198), a uncharacterized WD motif containing protein. Analysis of the unc-54(e190) null allele revealed that loss of unc-54 alone is sufficient to induce these ectopic membrane extensions, though not at the level of penetrance observed in GE6583. Fosmid rescue experiments using constructs containing either wildtype Y45E5B.2 or unc-54 were able to partially rescue the mutant phenotype, suggesting that the two genes are required to prevent ectopic muscle membrane extensions. We are currently in the process of characterizing Y54E5B.2 and determining why the loss of the unc-54 myosin results in these membrane extensions.

    Affiliations:
    - University Carolo-Wilhelmina of Braunschweig, Institute of Genetics, Braunschweig, Germany
    - Molecular and Cell Biology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, U.S.A.
    - Dept Zoology, Univ British Columbia, Vancouver, BC, Canada


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