Figure 8.

Model depicting the pathways through which scrib mutants promote tumorigenesis. (A) In scrib mutant cells, inappropriate aPKC activity leads to alterations in cell polarity/morphology and excessive cell proliferation that is restrained through JNK-dependent apoptosis. Although distinct aPKC and JNK-dependent pathways could be genetically separated in scrib mutants, it is possible that aPKC-dependent defects, refractory to aPKC^CAAXDN-mediated inhibition, still drive JNK activation. (B) Expressing Ras^ACT in scrib mutant cells blocks JNK-mediated apoptosis and unveils a role for JNK in promoting loss of differentiation, tumour overgrowth and invasion. aPKC signalling exerts only a minor role in promoting tumour overgrowth. (C) Expressing N^ACT in scrib mutant cells blocks differentiation and promotes JNK-mediated tumour overgrowth and invasion. aPKC signalling promotes tumour overgrowth through either increased cell proliferation or cell survival to counteract a JNK-dependent restraint on tumour overgrowth.