Effects suggest sds22 functions as an necessary positive regulator of PP1 to cell invasion and to maintain epithelial organization. To check whether these ectopic cells are sds22 mutant or wild type, we used the hsFLP/MARCM way to really level mutant cells with GFP. We discover that the Elav positive neurons in the optic stalk are also GFP positive, suggesting that purchase Fingolimod sds22 mutant cells are migrating away from the eye disc. In addition to photoreceptor cells, we also find undifferentiated cells and cone cells in the eye disc are mislocalized in the optic stalk, suggesting that the migratory behavior isn’t simply on account of photoreceptor axon extension. Another possibility is that the basal migration by sds22 mutant cells might be a second consequence of cell death. To test this, we blocked cell death by over-expression of p35 in sds22 mutant cells. Elav positive mutant neurons are still mislocalized in the optic stalk, showing that cell invasion is not a secondary consequence of cell death induced Plant morphology by lack of sds22. Together, these results claim that sds22 is required for maintaining proper cellular situation in both the eye disc and wing. Sds22 physically binds to Protein Phosphatase 1 and regulates PP1 activity 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 importance of this conversation has not been studied in vivo and the function of PP1 in epithelial integrity and cellular invasion isn’t clear. To discover the system of how loss of sds22 triggers cell attack like behavior, we first asked whether loss of PP1 activity causes a similar phenotype as loss of sds22. Drosophila has four PP1 isoforms, called after PP19C, PP113C, PP187B, theirsubtype and chromosome area, and PP196A. Of the, Imatinib price PP113C and PP196A aren’t essential depending on lack of function studies and for that reason weren’t contained in this study. We discover that loss of PP187B or PP19C share many features with loss of sds22, including loss of tissue architecture and difference, increased cell death and cell unpleasant behavior. We examined whether an identical relationship exists in Drosophila, because loss of sds22 phenotypes in yeast can be suppressed by high dose of PP1. Strikingly, overexpression of PP19C, although not PP187B, can somewhat suppress sds22 phenotypes. Over-expression of individual PP1 isoforms alone does not cause an evident phenotype. The myosin II regulatory light chain Spaghetti Squash is a primary target of PP1B9C and dephosphorylation of Sqh inactivates Myosin II. Phosphorylation of Sqh is enhanced in sds22 mutant string cells, suggesting that Sqh hyperphosphorylation might play a role in mediating phenotypes caused by loss in sds22. To try this hypothesis, we first ectopically expressed a phosphomimetic form of Sqh inside the eye disc using both the FLPout technique or ey GAL.