Fig. 4 Rbfox1l/Rbfox2 knockdown results in cardiac and skeletal muscle defects. (A, B) In Rbfox double morphants, myotomes are chevron-shaped as in control embryos (lateral view, one myotome is false-colored in each panel). (C–H) Polarized light microscopy reveals that rbfox1l/rbfox2 morphant muscle has delayed birefringence at 30 hpf (compare C with D) that partially recovers by 48 hpf (compare E with F). (G–I) Rbfox1l/Rbfox2 knockdown in myl7-GFP embryos that have GFP + myocardial cells, reveals cardiac muscle defects, with low rbfox1l/rbfox2 MO doses (1.5 ng each) causing ventricular defects and high doses (9 ng each) affecting the morphology of the entire heart. WT = mock-injected; MO = morpholino; a = atrium; v = ventricle. Scale bars = 100 μm (A–B; G–I), 500 μm (C–F).
Reprinted from Developmental Biology, 359(2), Gallagher, T.L., Arribere, J.A., Geurts, P.A., Exner, C.R., McDonald, K.L., Dill, K.K., Marr, H.L., Adkar, S.S., Garnett, A.T., Amacher, S.L., and Conboy, J.G., Rbfox-regulated alternative splicing is critical for zebrafish cardiac and skeletal muscle functions, 251-61, Copyright (2011) with permission from Elsevier. Full text @ Dev. Biol.