Posterior expansion of erythroid gene expression when FGF signaling is inhibited during gastrulation. (A) Blocking FGF signaling expands Scl expression into posterior regions in a dose-dependent manner (ventral views). Embryos were treated from stage 8 with increasing concentrations of SU5402: 25 μM (ii), 50 μM (iii), and 100 μM (iv), grown to stage 18/19 and probed along with control embryos (i) by whole-mount in situ hybridization for Scl expression. Control siblings were treated with 0.1× MBS containing 0.5% DMSO. (B) Blocking FGF signaling expands erythroid gene expression posteriorly but leaves endothelial and myeloid gene expression intact. Embryos were treated with 50 μM SU5402 from stage 8 and grown to stage 18/19 (anterior ventral views). Control embryos (i,iii,v,vii,ix,xi) in 0.1× MBS plus 0.5% DMSO and treated embryos (ii,iv,vi,viii,x,xii) were then probed by whole-mount in situ hybridization for Scl (i,ii), Lmo2 (iii,iv), Runx1 (v,vi), Fli1 (vii,viii), SpiB (ix,x), and Mpo (xi,xii). Numbers of embryos assayed is recorded in bottom right of each panel. (C) FGF signaling must be blocked during gastrulation for the expansion of Scl expression (anterior ventral views). Embryos were treated with 50 μm SU5402 from stages 7.5, 9, 10, and 11.5 (ii,iv,vi,viii) and grown along with untreated embryos (i,iii,v,vii) to stage 18/19. Embryos were probed for Scl expression by whole-mount in situ hybridization.