Figure 8.
The basement membrane and hemidesmosomal-like structures have an expanded distribution in the slow elongation mutants. Representative wild-type (A and E), spc-1(ra409) (B and F), sma-1(ru18) (C and G), and egl-19(st556) (D and H) embryos double labeled with perlecan antisera and MH4, an antibody that recognizes the intermediate filaments of the hypodermal hemidesmosomal-like structure. In wild-type embryos (A), perlecan is evenly distributed under each of the body wall muscle quadrants. Similarly, in spc-1 (α spectrin) (B) and sma-1 (βH spectrin) (C) mutants, perlecan is distributed evenly under each of the body wall muscle quadrants. However, the spatial distribution of perlecan in spc-1 and sma-1 mutants is wider than normal, reflecting the defects observed in the body wall muscle (Figs. 6 and 7). In egl-19 mutants (D), the distribution of perlecan is normal. In wild-type embryos, the hemidesmosomes have assemble under each of the body wall muscle quadrants (E). In spc-1 (F) and sma-1 (G) mutant embryos, the hemidesmosomes have assembled normally under each body wall muscle quadrant (F and G). However, the hemidesmosomes are assembled in an area wider than normal. In egl-19 mutants (H), the distribution of the hemidesmosomes is normal. Arrowheads indicate width of basement membrane (A–D) and hemidesmosomes (E–H). Bar, 10 μM.