Fig. 6.

Suppression of the tnnt3a progressive myofibrillar disorganisation phenotype in the absence of functional thick filaments. (A–D) Incubation with the myosin inhibitor blebbistatin: phalloidin staining of embryos incubated with DMSO reveals normal myofibrils in a control embryo (A) and the expected disruption in actin distribution in a tnnt3a MO-injected embryo (C). When embryos are treated with blebbistatin, loose myofibrils are observed in a control embryo (B) and wavy but striated myofibrils can be seen in a tnnt3a MO-injected embryo (D). Scale bars: 25 μm, insets are 2× magnifications of corresponding panels. (E–H) Analysis in the sloth mutant: a 48 hpf wild-type sibling displays normally striated fast fibres (E). In a wild-type sibling injected with the tnnt3a MO (F), myofibrils undergo degradation and actin becomes diffuse. In a sloth mutant embryo (G), actin is distributed in thick filament-free sarcomere-like blocks along myofibrils. In a sloth mutant injected with tnnt3a MO (H), actin remains in blocks rather than dispersed in the cytoplasm. Scale bars: 10 μm, insets are 2× magnifications of corresponding panels. All images are lateral views of a myotome. Confocal images were obtained from planes deep in the trunk musculature. Phalloidin staining is white and DAPI for nuclei is blue.