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Resources » Paper

Davide Faggionato et al. (2006) European Worm Meeting "Learning Lessons from dys-1 and snf-6 - Having Acetylcholine as a Teacher"

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  • Comments on Davide Faggionato et al. (2006) European Worm Meeting "Learning Lessons from dys-1 and snf-6 - Having Acetylcholine as a Teacher" (0)

  • Overview

    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00027572

    Davide Faggionato, Oyunbileg Nyamsuren, & Ralf Baumeister (2006). Learning Lessons from dys-1 and snf-6 - Having Acetylcholine as a Teacher presented in European Worm Meeting. Unpublished information; cite only with author permission.

    We study the function/dysfunction of mutations of genes that in humans have been associated with degenerative disorders. Recently, we identified components of an ubiquitylation complex as regulators of muscle assembly and turnover. Specifically, mutational inactivation of ubiquitylation suppressed paralysis of unc-45 mutant animals that show a severe myofibril disorganization 1.. In order to get an idea whether this is a generally applicable way to reduce the phenotypic consequences of mutations in muscle genes, we focused on other genes affecting muscle assembly and function.. dys-1 encodes the C. elegans orthologue of human dystrophin, mutations of the latter being responsible for Duchenne muscular dystrophy. One of the available mutants in dys-1, cx18, displays a surprisingly mild impairment of movement, that, however, is strongly enhanced in the background of hlh-1/MyoD, generating a synthetic paralysis. However, dys-1(cx18) animals also display subtle phenotypes like increased sensitivity to aldicarb, suggesting an additional neuronal function of this gene 2.. In a previous screen for ethanol resistance, mutations in the muscular sodium-acetylcholine cotransporter gene snf-6 were identified. Surprisingly, snf-6 mutations strongly resemble the dys-1 mutant phenotype in an hlh-1 background, suggesting a link between cholinergic signalling and dystrophin function.. In order to understand dys-1 dysfunction, we performed a detailed comparative analysis of both mutants and will present the data in our poster.. 1Hoppe T, Cassata G, Barral JM, Springer W, Hutagalung AH, Epstein HF, Baumeister R. Regulation of the myosin-directed chaperone UNC-45 by a novel E3/E4-multiubiquitylation complex in C. elegans. Cell. (2004) 118(3), 337-49. 2Bessou C, Giugia JB, Franks CJ, Holden-Dye L, Segalat L. Mutations in the Caenorhabditis elegans dystrophin-like gene dys-1 lead to hyperactivity and suggest a link with cholinergic transmission. Neurogenetics. 1998 Dec;2(1):61-72


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