(Downloading may take up to 30 seconds.
If the slide opens in your browser, select File -> Save As to save it.)

Click on image to view larger version.



Fig. 4. Genetic control of SMP formation. (A-C) Analysis of SMP formation in the asplenic mutants Dh and Bapx1–/–, using PDX1 antibody (red) and phalloidin (green) at E10. (A) Wild-type embryos show the characteristic triangular shape of the SMP and spleno-pancreatic mesenchyme, whereas in Bapx1–/– embryos (B), although the mesenchyme grows to the left, the triangular shape is compromised and the pancreatic bud remains near the embryonic midline (broken line). In the Dh/Dh embryos (C), the SMP is lacking and no obvious leftward growth is detected. At E10.5 in Bapx1–/– embryos (E), lateral growth occurs but to a lesser extent than in wild-type embryos (D), and the pancreas remains at the midline. (F,G) Analysis of SMP formation in Fgf10–/– embryos following staining for PDX1 (red), and with propidium iodide (green). Development of the pancreatic endoderm is severely compromised in the Fgf10–/– embryos, as revealed by an apparent loss of PDX1 staining in the mutant embryos (G). Despite this, leftward growth of the spleno-pancreatic mesenchyme and SMP occurs normally (G).