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Fig. 4. Pancreatic defects in PdxCre^early ß-cat^active correlate with changes in FGF and hedgehog signaling, and loss of Pdx1⁺ progenitor cells. (A-C) Whole-mount in situ hybridization. Fgf10 expression is downregulated in the dorsal pancreatic (dp) and ventral pancreatic (vp) mesenchyme of the PdxCre^early ß-cat^active mutants (C) at E10.5. Fgf10 expression within the pancreatic mesenchyme of PdxCre^late ß-cat^active mutants (B) is equivalent to control (A). s, stomach. (D-F) Immunohistochemical staining. Pancreatic sections at E12.5 stained for the hedgehog (Hh) receptor Ptch1 reveal increased levels of Ptch1 within the pancreatic epithelium (circled in blue) of the PdxCre^early ß-cat^active mutants (F) when compared with control pancreas (D). Ptch1 staining in PdxCre^late ß-cat^active (E) pancreatic sections is equivalent to control (D). (G-I) Pancreatic sections at E12.5 stained for Hh. The PdxCre^early ß-cat^active pancreatic epithelium (circled in blue, I) also exhibits increased levels of Hh when compared with control (G) and PdxCre^late ß-cat^active pancreas tissue (H). (J-L) Staining of E12.5 pancreata with E-cadherin (green) to mark the pancreatic epithelium and Pdx1 (red) reveals a dramatic loss of Pdx1+ progenitor cells in the PdxCre^early ß-cat^active mutants (L). By contrast, the PdxCre^late ß-cat^active (K) display Pdx1⁺ cell numbers that are equivalent to control (J). Scale bars: 50 µm in J-L.

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