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Resources » Paper

Hetherington , Suzannah et al. (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "The nematode-specific protein GEI-16/PAT-12 organizes and/or maintains fibrous organelle components at the apical membrane."

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  • Comments on Hetherington , Suzannah et al. (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "The nematode-specific protein GEI-16/PAT-12 organizes and/or maintains fibrous organelle components at the apical membrane." (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00036865

    Hetherington , Suzannah, Gally, Christelle, Fritz, Julie-Anne, Behm, Carolyn, & Labouesse, Michel (2010). The nematode-specific protein GEI-16/PAT-12 organizes and/or maintains fibrous organelle components at the apical membrane presented in C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany. Unpublished information; cite only with author permission.

    Morphogenesis of the Caenorhabditis elegans embryo is driven by the epidermis and requires input from the body wall muscles. Both tissues are mechanically coupled through trans-epithelial attachment structures called fibrous organelles (FOs). Here, we report the identification of a new FO component called GEI-16. We initially identified this gene through a RNA interference (RNAi) screen for potential anthelminthic drug targets. GEI-16 proved necessary for maintaining the tight link between muscles and the cuticle, since RNAi against gei-16 caused muscle and cuticle detachment. In parallel, w e demonstrated an interaction between the core FO component VAB-10A and GEI-16 by yeast two-hybrid analysis. We confirmed by RT-PCRs that gei-16 encodes at least 8 different transcripts, and identified two mutations in the gene, gei-16(tm2298) and pat-12(st430) that display embryonic elongation defects typical of FO-defective mutants and fail to complement. Hence we suggest that pat-12 and gei - 16 correspond to the same gene. We developed GFP-tagged fusion proteins for the main classes of transcripts and observed that one of them, which could rescue the embryonic lethality of both gei-16/pat-12 alleles, was specifically localized to FOs. Its absence specifically affected FO organization, particularly at the apical membrane where intermediate filaments, MUP-4 and VAB-10 stripes were lost. Consistent with this view, knockdown of IFs or VAB-10 induced GEI-16::GFP disorganization mostly at the apical side showing an interdependent localization of these FOs components. In contrast, basal markers like LET-805 or UNC-52 did not display major disorganization problem when gei-16/pat-12 was absent. Altogether our data suggest that GEI-16 could be an epidermal scaffolding protein responsible for the organization and/or maintenance of FOs mainly at the apical side during embryonic development.


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