Fig. 4

a The transgene uas:fgf8-T2A-cfp (under control of Gal4-ERT) and its marker Eos. b The two characteristic phenotypes observed at 24 hpf upon activation of the transgene. c Erk domain of activity visualized by IHC against phosphorylated Erk (pErk) at ten somites in non-activated embryos (left) or in embryos in which the transgene was activated from bud stage (right): the uniformly expressed exogenous Fgf8 enlarges the domain of activity of Erk to the whole embryo, but doesn’t alter the Erk activity gradient, Fig. S4. d Time variation of total fgf8 mRNA (RTqPCR data) in presence of an exogenous source of Fgf8. At time t = 0 (bud stage) the concentration of fgf8 is contributed by the endogenous one (continuous line: best linear fit y = 0.11 x + 1 with r² = 0.98). From then on, the endogenous concentration decreases (see Fig. 5) while the exogenous concentration increases: it typically doubles the initial endogenous concentration in 9 h (about 20 somite stage). Inset: gel displaying the increase in exogenous fgf8 mRNA at various times post activation versus a reference gene (β-actin). e Rates of PSM shrinkage (V_PSM), tail growth (V_tail), and wavefront velocity (V_front) in embryos (n = 17) in which an exogenous source of Fgf8 was turned on. The various rates are only mildly affected by the increase in Fgf8 due to the exogenous source.