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. 2010 May 3;189(3):527–539. doi: 10.1083/jcb.200912125

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© 2010 Etard et al.

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Figure 4. — Apo2a morphants have defective myosepta and form intersomitic giant myofibers. (A–C) DIC images of Mo(ATG)-apo2a–injected embryos. Mo(ATG)-apo2a morphants (Mo) exhibit cell-free spaces in the somites (A and B, stars), disrupted myosepta (B and C, arrows), and giant myofibers that span two somites (C, arrowhead). (D–F) Immunohistochemistry with antibodies directed against myoseptal proteins reveals defects in the myosepta of apo2a morphants: α-Dystroglycan (DG) staining of control (cont; D) and Mo(ATG)-apo2a–injected (Mo; E and F) embryos (white arrows, disrupted myosepta; green arrows, split myosepta). (G and H) Laminin staining reveals abnormal myosepta in Mo(ATG)-apo2a morphants (H) compared with wild type (G). Green arrows, split myosepta. (I–K) Double immunohistochemistry with anti–α-dystroglycan (DG) and the anti-slow muscle myosin antibody F59 reveals giant slow muscle myofibers (J, arrowhead) crossing the somite boundary (J, arrow). (I) Control embryos never show these intersomitic myofibers. Detachment of myofibers from the myosepta (K, arrow) generates cell-free spaces (K, star). (L and M) Sarcomeric myosin stained with A4.1025 in Mo(ATG)-apo2a morphants shows detached slow fibers (M, yellow arrows) overlaying fast fibers and generating cell-free areas inside the muscle tissue (star). Most of the fast fibers are still anchored to the myosepta. A few fast fibers have also detached (M, blue arrow). (L) Control. All embryos injected with Mo(ATG)-apo2a were coinjected with Mo-p53. Embryos are 72 h old. The anterior is shown to the left, dorsal side up. Bars, 25 µm.