Fig. 2

LiCl enhances neurogenesis in place of the IZ independently of canonical Wnt signaling and its effects are mimicked by Gsk3β inhibition. Zebrafish embryos analyzed at the 3- to 5-somite stage by in situ hybridization and flat-mounted, anterior up. (A-F′) Treatment with LiCl. At 80% epiboly (B,E,E′), treatment induces ectopic neurog1 expression in place of the MIZ (arrows in B,E′). LiCl posteriorizes the anterior neural plate when applied earlier (A), and is without effect when applied later (C). Bracket in A-D indicates the MIZ. (D,F,F′) Control. (G,H) Effect of LiCl applied at 80% epiboly (G, arrow) in transgenic hsp70l:tcf3-GFP^w3 embryos expressing a dominant-negative Tcf3a upon heat shock. Expression of this transgene alone does not perturb IZ formation (H). (I-L) The Gsk3β inhibitor OTDZT triggers ectopic neurog1 expression in place of the MIZ (I,I′, compare with J,J′), and within the LIZ when Her5 activity is reduced by her5GripNA injection (L, arrows, compare with K).