aPKCCAAXDN rescues scrib mutant morphology and proliferation defects, but does not prevent JNK-mediated apoptosis. eyFLP-induced MARCM clones (green). Grey scale is Elav (A-C, H, I), CycE (D), BrdU (E), TUNEL (F) and β-Gal to detect msn06946-lacZ enhancer trap activity (G). Phalloidin marks F-actin in red (A-C, H, I). A white bar indicates the location of the MF. (A-G) FRT82B scrib1 UAS-DaPKCCAAXDN. Expression of aPKCCAAXDN in scrib mutant clones rescues most cell morphology defects and normalizes the regular pattern of differentiation in the eye disc (A-C) with only occasional photoreceptor nuclei dropping basally at the edges of some mutant clones (arrow in B and C). The mutant cells no longer ectopically express CycE (D) or ectopically proliferate posterior to the MF (E), but the mutant cells still die as seen with TUNEL detection (F) and JNK signalling is still ectopically activated in some mutant tissue, as measured by the activity of the msn-lacZ enhancer trap (G). (H, I) UAS-scribbleFL19.2; FRT82B scrib1. Expression of a full-length Scrib transgene in scrib mutant clones completely rescues the mutant cell morphology defects as well as clonal tissue size throughout the eye/antennal disc.
Leong et al. BMC Biology 2009 7:62 doi:10.1186/1741-7007-7-62