In Drosophila, mutations in the Scribble complex trigger the formation of neoplastic tumors, which shares many regulatory and phenotypic commons with mammalian tumorigenesis. Through genetic screening, I identified several candidate genes regulating the scrib/dlg mutant tumor growth, including fog, which is an upstream regulator of non-muscle myosin II. The inhibition of Fog signaling induced accelerated growth of dlg mutant tumors, possibly through its regulatory function on myosin activity. Knockdown of myosin II components sqh and zip also lead to higher growth rate and larger tumor size in the dlg mutant tumors. Previous studies showed JNK signaling is a potential target of actomyosin activity. Our data suggested that Fogmyosin signaling may regulate the growth of nTSG mutation-indu...[ Read more ]

In Drosophila, mutations in the Scribble complex trigger the formation of neoplastic tumors, which shares many regulatory and phenotypic commons with mammalian tumorigenesis. Through genetic screening, I identified several candidate genes regulating the scrib/dlg mutant tumor growth, including fog, which is an upstream regulator of non-muscle myosin II. The inhibition of Fog signaling induced accelerated growth of dlg mutant tumors, possibly through its regulatory function on myosin activity. Knockdown of myosin II components sqh and zip also lead to higher growth rate and larger tumor size in the dlg mutant tumors. Previous studies showed JNK signaling is a potential target of actomyosin activity. Our data suggested that Fogmyosin signaling may regulate the growth of nTSG mutation-induced tumors through modulating JNK signaling activity.