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Background  Tumor Susceptibility Gene-101 (TSG101) promotes the endocytic degradation of transmembrane proteins and is implicated as a mutational target in cancer, yet the effect of TSG101 loss on cell proliferation in vertebrates is uncertain. By contrast,  Drosophila  epithelial tissues lacking the TSG101 ortholog  erupted  ( ept ) develop as enlarged undifferentiated tumors, indicating that the gene can have anti-growth properties in a simple metazoan. A full understanding of pathways deregulated by loss of  Drosophila ept  will aid in understanding potential links between mammalian TSG101 and growth control.    Principal Findings  We have taken a genetic approach to the identification of pathways required for excess growth of  Drosophila  eye-antennal imaginal discs lacking  ept . We find that this phenotype is very sensitive to the genetic dose of  stat92E , the transcriptional effector of the Jak-Stat signaling pathway, and that this pathway undergoes strong activation in  ept  mutant cells. Genetic evidence indicates that  stat92E  contributes to cell cycle deregulation and excess cell size phenotypes that are observed among  ept  mutant cells. In addition, autonomous Stat92E hyper-activation is associated with altered tissue architecture in  ept  tumors and an effect on expression of the apical polarity determinant  crumbs .    Conclusions  These findings identify  ept  as a cell-autonomous inhibitor of the Jak-Stat pathway and suggest that excess Jak-Stat signaling makes a significant contribution to proliferative and tissue architectural phenotypes that occur in  ept  mutant tissues.

Genetic Interactions between the Drosophila Tumor Suppressor Gene ept and the stat92E Transcription Factor