Fgf8 drives progression from myf5 to myod expression in the lateral somite. (A) Flatmounts of whole-mount in situ mRNA hybridisation for myod, myf5 and myogenin at 15 s in unmanipulated control, Fgf8 MO-treated, SU5402-treated and ace mutant embryos. In each panel, the entire posterior embryo is shown on the right in dorsal view, anterior upwards. On the left the youngest somites are magnified. Residual medial MRF expression is indicated (black arrows) adjacent to adaxial slow muscle cells (white arrowheads). The lateral extent of intersomitic border is marked (red dots) revealing the loss of lateral myod, and reduction in myogenin, but retention of myf5. Tailbud myf5 signal is lost in some Fgf8 MO and all SU5402-treated embryos (green arrowheads, whole mount insets, mildly affected individuals) but not in ace, and the narrowing of the tail of ace mutant on Kwt background with the intersomitic borders angled more sharply to the posterior (green arrows). (B,C) Myod expression 3 hours after implantation of Fgf8 or control beads at 10 s in unmanipulated (B) or Fgf8 MO-injected (C) embryos. Bead centres (X) and sizes (circle) relative to high- and low-magnification panels are indicated.
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