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Resources » Paper

Tylon Stephney et al. (2002) East Coast Worm Meeting "Alae Mutant Defects Assessed by SEM and TEM"

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00010287

    Tylon Stephney, Carolyn Marks, Adam Hartley, Min Ren, Charles S Rubin, & David H Hall (2002). Alae Mutant Defects Assessed by SEM and TEM presented in East Coast Worm Meeting. Unpublished information; cite only with author permission.

    We have previously reported movement defects in adult C. elegans after RNAi (dsRNA feeding) with the gene PKC4, which encodes a novel Ser/Thr protein kinase (Ren et al., 2001). The PKC4 protein is expressed highly in the seam cells in late-stage embryos and again in late L4 stage, at the time of morphogenesis for seam-cell derived cuticular structures, the alae. It seemed likely that the movement defects, a sloppy zig-zag body motion of variable amplitude when placed on standard agar plates, were the result of absent or poorly formed alae. We have fixed adult animals for examination by scanning electron microscopy (SEM) and transmission electron microscopy (TEM) and compared these PKC4 RNAi animals to adult wild type. We will show SEM evidence for the normal extent of adult alae and several other hallmark features of the body surface, and TEM data for the corresponding seam cell cytology which underlies the alae. As predicted, the "knockout" animals often show alae defects or complete loss of alae locally, with a penetrance which agrees well with the prevalence of movement defects. The most common defect is a merger of the tripartite ala structure into a large smooth ridge of cuticle, or less often, a zone of smooth cuticle with no ridge at all. In severely affected PKC4 RNAi animals, some tissue defects can be seen in seam cells, including cell swelling and general disorder in the cytoplasm.


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