Fig. 6. upd activates the JAK/STAT pathway in cells posterior to the small intestine. Sagittal sections through the hindgut at stages 11 (A) and 12 (B) show outlines of the everting renal tubules (black dashes), small intestine primordium (red dots), large intestine primordium (yellow dots) and rectum primordium (orange dots). Estimates of the lengths of the small intestine (SI) and the large intestine (LI) are shown based on analysis of the sets of serial sections to which A and B belong. Scale bar: 50 µm. Levels of Stat92E protein and mRNA are barely detectable in upd^os1A embryos (C and E, respectively), but dramatically upregulated in bynGAL4; UAS-upd embryos (D and F, respectively); Stat92E protein is also upregulated in bynGAL4, UAS-hop^TML embryos (L). Stat92E protein is detected along a significant region of the length of the anterior hindgut, as observed in both whole-mount (G,I) and sagittally sectioned embryos (H,J) at stages 11 (G,H) and 12 (I,J). The hindgut is outlined by black dots (H,J), and red dots indicate the observed anteroposterior gradient of Stat92E protein (H,J). Consistent with this, double staining for both upd mRNA (in situ hybridization) and Stat92E protein (antibody staining) shows expression of Stat92E in an anterior-to-posterior gradient (brown, posterior extent marked with open arrowheads) that extends posterior to the domain of upd expression (blue, posterior extent marked with black arrowheads) (K). Expression of UAS-upd with drmGAL4 in an upd mutant background rescues the upd hindgut elongation defect (M), while expression of UAS-hop^TML with drmGAL4 in an upd mutant background fails to rescue (N); Crb is used to outline hindgut morphology. In C-G,I, the lumen of the hindgut is indicated with dots; the anterior limit of the small intestine is indicated with a larger dot.