Figure 8.

The effect of smyd1a deficiency on sarcomere organization in slow muscle fibers. Zebrafish embryos of WT sibling, smyd1a^mb4, smyd1a^mb5, Myom3^mn0067gt, Myom3^mn0067gt; smyd1a^mb4, and Myom3^mn0067gt; smyd1a^mb5 embryos were fixed at 24 hpf. The sarcomere organization was analyzed by immunostaining with the anti-MyHC (F59) antibody (A–C), direct observation of Myom-3-RFP localization (D–F), and TEM analysis (G–I). Lateral view of myosin thick filament organization in slow muscle fibers (A–C) of WT control (A), smyd1a^mb4 (B), and smyd1a^mb5 (C) mutant embryos by F59 antibody staining at 24 hpf. Lateral view of M-line organization of Myom-3-RFP in slow fibers of Myom3^mn0067gt (D), Myom3^mn0067gt; smyd1a^mb4 (E), and Myom3^mn0067gt; smyd1a^mb5 (F) mutant embryos at 24 hpf. TEM analysis shows the sarcomere organization in slow myofibers of WT control (G), smyd1a^mb4 (H), and smyd1a^mb5 (I) mutant embryos at 48 hpf. Scale bars: 30 µm (A, D); 500 nm (G).