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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.
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