Figure 2

Loss of scrib/dlg function in FCs at the posterior disrupts the EGFR signaling. Wild type (A, D, E, G and H) and mosaic egg chambers with scrib² (B, F and I) or dlg^m52 (C and J) clones at the posterior, marked by the absence of nuclear GFP (green in B, C, F and I) or β-gal (green in J), stained for nuclei (DAPI, blue), β-gal (red in A-C), DG (red in D-F) or dp-ERK (red in G-J). (A-C) In the wild type, expression of kek enhancer trap marker BB142 can be observed in the PFCs at stage 6-8 egg chambers (A). Expression of BB142 is completely absent in the scrib² (B-B") and dlg^m52 (C-C") clone cells at stage 8 egg chamber. (D-F) In the wild type, DG is evenly expressed in all FCs before stage 6/7, when DG is down regulated in the PFCs (D, D'). At stage 9/10, DG expression is dramatically reduced in all FCs except the AFCs (E, E'). Remarkably, ectopic expression of DG in all cell-membrane domain is evident in the scrib² multilayered clone cells at stage 9/10 chambers (F-F"). (G-J) In the wild type, dp-ERK can be detected in the posterior FCs from stage 6-8 (G, G', H and H'), and in dorsal FCs at stage 9 (H, H'). ERK activation can still occur in scrib² (I-I") or dlg^m52 (J-J") mutant posterior FCs at stage 6 egg chamber.