Fig. 8. Three-step model for endoderm-mesoderm cross-talk controlling formation of the zebrafish ventral pancreatic bud. (A) First phase, 26-29 hpf. Early fgf24 expression within the region of the endoderm (orange) that will give rise to the pancreatic ventral bud patterns the adjacent LPM (green) into the pancreatic LPM. erm is a probable direct Fgf24 transcriptional target within the LPM. The pancreatic LPM is characterized by pea3, erm, isl1, meis3, fgf24 and fgf10 expression. fgf10 (light gray) is weakly expressed in the pancreatic LPM at these stages. (B) Second phase, 29-32 hpf. The pancreatic LPM triggers the induction at 32 hpf of ptf1a expression in endodermal cells (ptf1a-positive cells schematized in blue). fgf24 expression is restricted within the pancreatic LPM and, at the same time, fgf10 expression increases in the same tissue. pea3 and erm expression in the pancreatic LPM indicates that FGF signaling is active in this tissue. As SU5402 exposures after 26-29 hpf do not abrogate ventral bud specification, this suggests that this step is FGF-independent (signal X and white arrow). fgf10 and fgf24 are functionally redundant in patterning the pancreatic LPM, and therefore in specifying the ventral bud. At the same time, fgf24 expression disappears from the pancreatic endoderm and both fgf10 and fgf24 are expressed in the pancreatic LPM. (C) Third phase, after 32 hpf. Since SU5402 treatments after ventral bud specification limit the size of the exocrine tissue, we propose that FGF genes, perhaps fgf24 and fgf10, could be involved in mesoderm-to-endoderm communication promoting ventral pancreas growth. DB, dorsal pancreatic bud; VB, ventral pancreatic bud.