The lethality and mutant phenotypes could be fully saved by a genomic rescue construct and an UAS sds22 transgene, suggesting that sds22 is the gene responsible for the observed phenotypes. sds22 homozygotes die at or prior to the first larva instar. To check whether loss of sds22 promotes tumefaction growth and metastasis of RasV12 expressing cells, we expressed RasV12 in sds22 mutant cells utilizing the eyFLP/MARCM Gemcitabine 122111-03-9 system, where 30% of a person’s eye is usually made up of mutant tissue. In keeping with previous studies, RasV12 overexpression alone triggers civilized over-growth but cells never invade in to the nearby ventral nerve cord or other tissues. Such animals can grow as larvae for 15 days after egg-laying and die ahead of pupation or as early pupae, when RasV12 overexpression is along with homozygous loss in sds22. In contrast, animals revealing RasV12 alone can only grow as larvae for up to 9 days AEL and then die as early pupae. At seven days AEL, we observe extensive hyperproliferation in eye discs of RasV12sds22 / animals but GFP positive cells are seen in the VNC at only low frequency. At 15 days AEL we find significant variety of ectopic Mitochondrion GFP positive cells spreading from a primary tumefaction within the brain into the VNC. In addition, as RasV12sds22 / tumors increase, the 2 eye antennal disks may actually merge in to one large mass. Together, these results suggest that lack of sds22 can co-operate with RasV12 to advertise invasive behavior and cyst development in a time dependent manner. Next, we asked whether the sds22 mutation alone is enough to cause cyst growth or metastasis. Similar to cells mutant for the neoplastic tumefaction suppressor genes scrib, dlg or lgl, we realize that sds22 mutant clones tend to be more sensitive to cell opposition, present k63 ubiquitin cell apoptosis, and don’t over proliferate or metastasize. The position of Ras signaling in promoting cell survival has been well-documented. We coexpressed the baculovirus caspase inhibitor p35 in sds22 mutant cells using the eyFLP/MARCM program to block cell death, to test perhaps the cooperative effect between loss of sds22 and Ras overexpression is related to cell survival. Curiously, these undead cells induce equally cell autonomous and non cell autonomous cellular growth and result in a enormously over-grown and folded eye disc and enlarged tumor like adult eyes, indicating that loss of sds22 confers tumor development when cell death is inhibited. Overexpression of p35 alone does not cause any obvious development disorders. But, we do not discover GFP labeled cells outside of the eye antennal disc/optic lobe region, suggesting that blocking cell death is not sufficient to market metastasis of sds22 / cells. Combined with the overgrowth phenotype in cooperation with oncogenic Ras, these effects suggest that sds22 mutant cells induce uncontrolled proliferation when combined with another genetic change or hit that promotes cell survival. Provided that tumor suppressor mutations often require a second hit to express their full phenotypes, these data suggest that sds22 is just a new Drosophila tumor suppressor gene.