Fig. 10

Fig. 10

Stage-specific disruption of RA during neural crest entry and migration along the foregut, but not thereafter, leads to colonization defects. (A-D) Maximum intensity confocal projections reveal Hu⁺ neurons in lateral views of the gut at 73 hpf in (A) Control larvae (DMSO treated), and larvae treated with DEAB from (B) 28–36 hpf, (C) 36–48 hpf, and (D) 48–73 hpf. Scale bar: 70 μM (E) Bar graphs depicting the percentage of larvae exhibiting normal colonization (neurons along whole length of gut), partial colonization (neurons present to the midgut) and no colonization (no neurons along the gut). (F) Cartoon illustration of the role of RA and Meis3 during enteric colonization of the gut. RA (cyan) is synthesized along the foregut mesenchyme (beige) concomitant with enteric neural crest (green) entry into the gut from the vagal neural crest domains. Meis3, functionally downstream of RA in the neural crest, and/or RET regulate caudal colonization of the gut during enteric nervous system development. The action of RA affects enteric colonization primarily during early foregut migration phases (28–48 hpf).