Fig. 3
Hedgehog signalling plays a central role during larval tail regeneration. a Continuous treatment with the Hedgehog pathway inhibitors cyclopamine (20??M) and LDE225(20??M) blocks regeneration (Cyclopamine 10/10, LDE 10/10, number of experiments?=?2) (Control 20/20, number of experiments?=?4). Cyclopamine pulse treatment blocks regeneration (8/10, number of experiments?=?2). b Larvae treated with cyclopamine (20??M) and LDE225 (20??M) from 0 to 48 hpe have reduced expression of dlx5a and msxc (for all panels results are 10/10, number of experiments?=?2). c Wound-induced expression of markers for the Wnt/?-Catenin, FGF and RA pathways is lost after treatment with cyclopamine. Larvae in the wnt10a and pea3 panels were treated with 50??M cyclopamine from 0 to 30 hpe. tcf7, fgf10a and raldh2 panels were treated with 20??M cyclopamine from 0 to 48 hpe (for all panels results are 10/10, number of experiments?=?2). d Cell proliferation is inhibited by treatment with cyclopamine (control n?=?10, cyclopamine n?=?8, number of experiments?=?2). This analysis was done as in Fig. 1d. Unpaired t test two-tailed results in P?<?0.0001 indicated as ****. e Upregulation of Wnt/?-Catenin signalling after cyclopamine treatment restores expression of dlx5a, msxc and raldh2 (for all panels results are 10/10, number of experiments?=?3). Arrowheads indicate partial rescue of marker expression. Larvae were treated from 0 to 40 hpe with 50??M cyclopamine and then incubated in 10??M GskXV until fixation