Abstract
Abstract Transaldolase is the rate-limiting enzyme in the non-oxidative branch of pentose phosphate pathway. Though transaldolase deficiency has been implicated in enhancing apoptosis in cell culture, yet there is no reported genetic phenotypic study of transaldolase knockdown mediated apoptosis in Drosophila. Here, we showed the novel phenotypes, the posterior bulgy eye and the shrunk wing, upon RNAi knockdown of transaldolase by eye-specific GMR-Gal4 and wing-specific MS1096-Gal4 drivers respectively. Biochemical analysis by acridine orange and TUNEL assay confirms the phenotypes are due to apoptosis. To further genetically confirm the phenotypes are due to apoptosis, we knockdown each of the apoptosis-related genes, JNK,p53, hid, and Dronc, simultaneously in the transaldolase knockdown flies, which revert the phenotypes back to normal, suggesting the specific phenotypes by the transaldolase knockdown are triggered by apoptosis. Neuronal expression of transaldolase regulates lifespan in Drosophila. We have generated the GMR-Gal4>UAS-Tal RNAi homozygous viable line to screen about 400 RNAi knockdown fly lines for the modifiers either suppressing and enhancing the bulgy apoptotic eye by transaldolase knockdown. We have identified a number of novel modifiers which genetically interact with the transaldolase knockdown induced apoptosis. The information may provide more new novel molecular targets for the treatment and prevention of transaldolase-related metabolic diseases and cancer.