Figure 9.

The effect of smyd1a deficiency on sarcomere organization in fast muscle fibers. Zebrafish embryos of WT sibling, smyd1a^mb4, and smyd1a^mb5 mutant embryos were fixed at 48 or 72 hpf. The key sarcomere structures were analyzed by staining with Phalloidin-TRITC and various antibodies, as well as TEM. A–C) Lateral view of myosin light chain organization in fast muscle fibers of WT control (A), smyd1a^mb4 (B), and smyd1a^mb5 (C) mutant embryos shown by anti-MyHC (MF20) antibody staining at 72 hpf. D–F) Lateral view of myosin light chain organization in fast muscle fibers of WT control (D), smyd1a^mb4 (E), and smyd1a^mb5 (F) mutant embryos shown by anti-MyLC (F310) antibody staining at 48 hpf. G–I) Lateral view of M-line organization in fast muscle fibers of WT control (G), smyd1a^mb4 (H), and smyd1a^mb5 (I) mutant embryos by anti-Myomesin antibody staining at 48 hpf. J–L) Lateral view of Z-line organization in fast muscle fibers of WT control (J), smyd1a^mb4 (K), and smyd1a^mb5 (L) mutant embryos by anti-α-actinin antibody staining at 48 hpf. M–O) Lateral view of actin thin filament organization in fast muscle fibers of WT control (M), smyd1a^mb4 (N), and smyd1a^mb5 (O) mutant embryos analyzed by Phalloidin-TRITC staining at 48 hpf. P–R) TEM analysis shows the sarcomere organization in fast myofibers of WT control (P), smyd1a^mb4 (Q), and smyd1a^mb5 (R) mutant embryos at 48 hpf. Scale bars: 40 µm (A, D, G, J, M); 500 nm (P).