results suggest sds22 functions being an crucial positive regulator of PP1 to maintain epithelial organization and to dam cell invasion. To check whether these ectopic cells are sds22 mutant or wild-type, we used the hsFLP/MARCM way to absolutely tag mutant cells with GFP. We discover that the Elav positive neurons in the optic stalk are also GFP positive, suggesting that Icotinib ic50 sds22 mutant cells are migrating away from the eye disc. Additionally to photoreceptor cells, we also discover undifferentiated cells and cone cells in a person’s eye disc are mislocalized in the optic stalk, suggesting the migratory behavior is not only as a result of photoreceptor axon extension. Still another possibility is the migration by sds22 mutant cells may be a second consequence of cell death. To test this, we blocked cell death by over-expression of p35 in sds22 mutant cells. Elav good mutant neurons are still mislocalized in the optic stalk, suggesting that cell invasion is not another consequence of cell death induced Cholangiocarcinoma by lack of sds22. Together, these results suggest that sds22 is needed for maintaining proper cellular situation in the eye disc and wing. Sds22 actually binds to Protein Phosphatase 1 and regulates PP1 action in yeast and mammalian cells. Binding of the Drosophila homolog of Sds22 to PP1 subunits in addition has been confirmed in a yeast two hybrid system and Drosophila S2 cells. But, the functional significance of this interaction has not been studied in vivo and the position of PP1 in epithelial integrity and cellular invasion is not clear. To discover the system of how loss of sds22 causes cell invasion like behavior, we first asked whether loss of PP1 activity causes the same phenotype as loss of sds22. Drosophila has four PP1 isoforms, called after theirsubtype and chromosome site, PP19C, PP113C, PP187B, and PP196A. Of the, PP196A and CX-4945 price PP113C aren’t essential centered on lack of function studies and for that reason weren’t a part of this study. We realize that loss of PP187B or PP19C share many characteristics with loss of sds22, including loss of difference and tissue architecture, enhanced cell death and cell unpleasant behavior. Because loss of sds22 phenotypes in yeast might be suppressed by high dosage of PP1, we tested whether the same relationship exists in Drosophila. Amazingly, over-expression of PP19C, but not PP187B, can significantly suppress sds22 phenotypes. Over-expression of specific PP1 isoforms alone does not cause an obvious phenotype. The myosin II regulatory light chain Spaghetti Squash is a direct goal of PP1B9C and dephosphorylation of Sqh inactivates Myosin II. Phosphorylation of Sqh is increased in sds22 mutant follicle cells, suggesting that Sqh hyperphosphorylation might play a role in mediating phenotypes due to loss in sds22. To check this hypothesis, we first ectopically indicated a phosphomimetic form of Sqh within the eye disk using both the FLPout approach or ey GAL.