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Fig. 6. Absence of acetylcholine receptors in nic1 mutants disrupts myofibril organisation. Immunostaining with antibody F59 was performed to reveal slow muscle fibres in (A,B) 24 hpf and (C) 48 hpf wild-type embryos and (D,E) 24 hpf and (F) 48 hpf nic1 embryos. (C,F) Insets show cross section of slow muscle myosin in anterior trunk of embryo at 48 hpf. Myofibrils organisation was disrupted in the mutants (arrows). Bars (A,D) 20 µm, (B,E) 10 µm and (C,F) 50 µm. (G) Fibre length/somite width was significantly longer in mutant embryos (light-grey bars, n=22 at 24 hpf and n=13 at 48 hpf) compared with wild-type embryos (dark-grey bars, n=24 at 24 hpf and n=26 at 48 hpf; ±s.e.m., ***P<0.0001, unpaired t-test). Dual immunostaining with phalloidin and antibody F59 revealed striations in (H) wild type and (I) homozygote nic1 embryos at 48 hpf; bar 20 µm. Electron micrographs of longitudinal sections through axial muscles of the trunk of (J) wild type and (K) nic1 embryos at 48 hpf. Bars, 1 µm.

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