Fig. 7

Fig. 7 Residual fast fibres after Myf5 plus Myod knockdown are hedgehog dependent. In situ mRNA hybridisation (A,B) and immunofluorescent confocal stacks (C) of 23 ss, 24-26 hpf wild-type, Tg(mylz2:GFP) or myf5^+/hu2022 incross embryos. Lateral views, anterior to left. (A) Cyclopamine (CyA) treatment of embryos from a myf5^+/hu2022 incross injected with myod MO ablates residual myhz1 expression (arrows, magnified in insets). Fast muscle still forms in the absence of Myod and Hh signals. Note the altered somite shape, paralleling the absence of slow fibres. (B) Expression of eng1a and eng2a (arrowheads) is missing from myf5^hu2022 mutants injected with myod MO and is reduced in myod+myog double morphants. Eng1a is not affected by myf5 mutation (revealed by weak myf5 mRNA expression) or myod MO alone, although eng2a is drastically reduced in the myod morphant. (C) Tg(mylz2:GFP) embryos injected with myod MO show reduction of both the weak Engrailed protein in MFF nuclei (yellow arrowheads) and the strong Engrailed expression of muscle pioneers (blue arrowheads). (D) Schematic illustrating how the cells generated in medial and lateral modes of myogenesis in the early zebrafish somite (left) each contribute to several later compartments (right). Note that dermomyotomal contributions are not defined because cell lineage is largely unknown.