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<p>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 <i>Drosophila melanogaster</i>. Hypermorphic and hypomorphic alleles of <i>taxi</i> 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 <i>Adar</i> significantly rescued the reduction in lifespan caused by <i>taxi</i> overexpression in neurons. Conversely, the knockdown of <i>Adar</i> rescued the defective lifespan caused by <i>taxi</i> knockdown in neurons. We show that enzymatically inactive Adar also rescued the reduced lifespan in flies having a neuronal <i>taxi</i> 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 <i>taxi</i> and its interacting partner <i>Adar</i> is imperative in lifespan maintenance.</p>

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Neuronal expressions of Taxi and Adar are crucial in maintaining the lifespan of Drosophila melanogaster

  • 期刊论文

  • 发表日期：

    2025年11月17日

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  • Upasana Gupta,
  • Vanlalrinchhani Varte,
  • Fathima M. Ashraf,
  • Upendra Nongthomba

摘要

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.