Figure 5 Transcommitment to pancreatic lineage by misexpression of Ptf1a in the prospective stomach, duodenum, and CBD at E11.5.
Macroscopic views of embryos stained with X-gal at E11.5 (A–D; C and D are magnified views of the boxes in A and B). (A and C) Ventral and dorsal pancreatic buds and central nervous system (42, 43) were X-gal positive in control mice. Note that misexpression of Ptf1a was observed in patchy areas of the prospective stomach (arrows in D) and duodenum (arrowhead in D) in Hes1–/–Ptf1acre/wtROSA26r mice (B and D). (E–T) Histological analyses of the same samples shown in A and B. Patchy misexpression of Ptf1a was observed in the prospective stomach (arrow in F) and duodenal epithelium (arrows in H) in Hes1–/–Ptf1acre/wtROSA26r mice. (J) The CBD did not form at all, but instead is replaced by X-gal–positive aggregated cells in Hes1–/–Ptf1acre/wtROSA26r mice. Laminin immunostaining shows evagination from the stomach epithelium in Hes1–/–Ptf1acre/wtROSA26r mice (arrowheads in F and L). (N and P) The evaginated cells consisted of a large number of X-gal–negative, Pdx1-negative early glucagon-positive cells. Note that the proximal stomach epithelium was negative for Pdx1 (dotted lines in O and P). X-gal was ectopically observed in the Cdx2-positive duodenal epithelial cells (inset in R). (S and T) The DBA-positive CBD was replaced by DBA-negative, X-gal–positive tissue. Li, liver; PV, portal vein; dp, dorsal pancreatic bud; vp, ventral pancreatic bud. Scale bars: 50 μm. Original magnification, ×20 (A and B), ×80 (C and D).