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Fig. 1. Mutation of unc-94/tmd-1 causes severe disorganization of actin filaments in body-wall muscle. (A) Genomic organization of the unc-94/tmd-1 gene. Exons are indicated by boxes. Two alternatively spliced isoforms are generated as described (Stevenson et al., 2007). The position of the unc-94/tmd-1(tm724) deletion is indicated. (B) Western blot analysis of the TMD-1 protein in wild-type and unc-94/tmd-1(tm724) adult worms. The bands at 68 kDa (arrow) are not related to the TMD-1 protein (Stevenson et al., 2007). Anti-actin antibody was used to monitor equal loading of the protein samples. (C) Actin filaments in embryos (a,b) and adults (c,d) were visualized by staining with tetramethylrhodamine-phalloidin in wild-type (a,c) and unc-94/tmd-1(tm724) (b,d). Bars, 10 µm. (D) Organization of -actinin (a-f) and myosin (g-l) in body-wall muscle. Wild-type (a-c and g-i) or unc-94/tmd-1(tm724) (d-f and j-l) were immunostained for actin (a,d,g,j) and -actinin (b,e) or MyoA myosin heavy chain (h,k). Merged images are shown in c, f, i and l (actin in red and -actinin or MyoA in green). Arrows indicate positions of actin aggregates where -actinin or myosin did not localize. Bar, 10 µm.

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