These quantitative data showed that both the development of CagA induced apoptosis observed with coexpression of ectopic Bsk, and its withdrawal upon appearance of BskDN were statistically significant. A negative feedback loop in the JNK pathway. in order to Fingolimod cost further study the genetic relationship between CagA and JNK signaling, we applied a lacZ reporter allele of puckered , the main component. This construct is used extensively as a read-out for JNK pathway activation in Drosophila tissue using antibody staining for t galactosidase. Expressing CagA in combination with puc lacZ in the dorsal wing imaginal disk demonstrated that cells adjacent to those undergoing apoptosis are triggering JNK signaling. Upregulation of puc lacZ correlated with phosphorylation of JNK, confirming that specific activation of JNK signaling results from CagA expression. These data offer additional evidence that CagA term invokes JNK signaling in the wing imaginal disc epithelium. JNK Plastid signaling is triggered by a complex pair of signals including TNF and lack of epithelial polarity. . To look at the mechanism by which CagA initiates JNK signaling, we used the bx GAL4 driver to express CagA in conjunction with RNAimediated knockdown of identified epithelial polarity determinants and examined wing imaginal discs for improvement of the apoptosis phenotype. We tested a panel of polarity proteins, many of which caused apoptosis when knocked down in the lack of CagA expression. We chose to target a protein from each one of the previously described processes whose localization JZL 184 and function create epithelial cell polarity, and to simplify our analysis we picked polarity proteins that did not cause an apoptosis phenotype when knocked down on their own. When examined in conjunction with CagA expression, we discovered that RNAi mediated knockdown of neither the junctional protein Bazooka, nor the protein Crumbs enhanced apoptosis. In inclusion, knock-down of Par1, which has been shown to communicate with CagA in tissue culture cells, did not improve the phenotype caused by CagA term in this context. Apparently, RNAi mediated knockdown of the protein Discs Large didn’t cause a significant phenotype but considerably enhanced the apoptosis due to CagA appearance. The same result was seen with knockdown of Lethal Giant Larvae, another protein. The genes encoding these polarity proteins are known as neoplastic tumor suppressor genes since their loss causes tumor formation in Drosophila, and producing clones of cells which lack this type of class of polarity determinants is shown to induce JNK dependent apoptosis in imaginal discs. Our data suggest that nTSGs usually suppress CagAmediated JNK pathway activation and subsequent apoptosis within the wing imaginal disc. Disruption of the nTSGs stimulates JNK signaling through endocytosis of the TNF homolog Egr.