Expressing BskDN and aPKCCAAXDN in scrib mutant clones fully rescues the mutant phenotype. eyFLP-induced MARCM clones (green). Grey scale is Elav (A-C, F, G) and BrdU (D, E). Phalloidin marks F-actin in red (A-C, F, G). A white bar indicates the location of the MF. (A) FRT82B scrib1 UAS-DaPKCCAAXDN UAS-P35. Co-expression of P35 with aPKCCAAXDN in scrib mutant clones does not dramatically increase mutant tissue viability and results in non-cell autonomous tissue folding, and rounded cell morphology in some mutant cells (arrow). (B-D) FRT82B scrib1 UAS-DaPKCCAAXDN UAS-bskDN. Co-expression of BskDN with aPKCCAAXDN in scrib mutant clones rescues the mutant cell morphology and viability defects in both eye and antennal disc regions (B, C) and restores the normal pattern of cell proliferation posterior to the MF (D). (E-G) FRT82B UAS-DaPKCCAAXDN UAS-bskDN. Co-expression of BskDN with aPKCCAAXDN in clones has no discernible effect on cell proliferation (E) or cell morphology and differentiation (F, G).
Leong et al. BMC Biology 2009 7:62 doi:10.1186/1741-7007-7-62