Fig. 9

Fig. 9 Hsf1 activated heat shock stress response has a protective role in myofiber organization in smyd1b−/− mutant embryos. (A–H) Myofiber organization of slow muscles was analyzed using anti-myosin antibody (F59) staining in WT control (A, E), hsf1−/− mutant (B, F), smyd1b−/− mutant (C, G) and hsf1−/−; smyd1b−/− double-mutant (D, H) embryos at 28 hpf (A–D), and 48 hpf (E–H), respectively. Compared with the WT control (A, E), loss of Hsf1 function has no visible effects on myofiber organization in hsf1−/− mutant embryos (B, F). In contrast, loss of Smyd1b function significantly disrupted the myofiber organization in smyd1b−/− mutant embryos at 28 hpf (C). By 48 hpf, myofiber organization appeared to be improved (G). However, this improvement was significantly diminished in the hsf1−/−; smyd1b−/− double-mutant embryos at 48 hpf (H). (I–L) Myofiber organization of fast muscles was analyzed using anti-myosin antibody (MF20) staining in WT control (I), hsf1−/− mutant (J), smyd1b−/− mutant (K) and hsf1−/−; smyd1b−/− double-mutant (L) embryos at 72 hpf. Scale bars = 50 μm.