Abstract
Ageing involves deterioration in physiological processes, such as maintenance of neuronal health, muscle, fat bodies, and gut bacteria, which play a crucial role in the progression of ageing. In this study, we show that the expression of Taxi, a transcription factor is required to maintain the lifespan in Drosophila melanogaster. Hypermorphic and hypomorphic alleles of taxi show reduced lifespan. We have identified that pan-neuronal overexpression and knockdown of Taxi lead to a stark reduction in the lifespan. In our previous study, we showed that Taxi negatively regulates Adar. Interestingly, overexpression of Adar significantly rescued the reduction in lifespan caused by taxi overexpression in neurons. Conversely, the knockdown of Adar rescued the defective lifespan caused by taxi knockdown in neurons. We show that enzymatically inactive Adar also rescued the reduced lifespan in flies having a neuronal taxi overexpression background. Our work suggests that, besides the editing activity, Adar may have editing-independent roles implicated in lifespan regulation. Overall, we show that neuronal tissue-specific controlled expression of taxi and its interacting partner Adar is imperative in lifespan maintenance.
