Abstract
During the larval-prepupal transition in Drosophila, a balancing crosstalk occurs between autophagy and caspase activity in the remodeling fat body: the inhibition of autophagy induces caspase activity and the inhibition of caspases induces autophagy. Both autophagy and caspase activity are induced by a pulse of molting hormone (20-hydroxyecdysone, 20E) via the 20E nuclear receptor complex, EcR-USP. We here demonstrate that E93, a 20E primary-response gene encoding an HTH transcription factor, predominantly transduces 20E signaling to induce autophagy and caspase activity in the remodeling fat body. RNAi knockdown or mutation of E93 blocks autophagy and caspase activity, E93 overexpression induces them both, while E93 overexpression has a better rescuing effect on the inhibition of autophagy than caspase activity caused by EcR(DN) overexpression. At the transcriptional level, E93 not only greatly impacts the 20E-triggered transcriptional cascade, but also upregulates essential autophagy and apoptosis genes. Meanwhile, at the phosphorylational level, E93 blocks the PI3K-TORC1 signaling to initiate autophagy. Taken together, we conclude that autophagy and caspase activity are induced by 20E and predominantly transduced by E93 in the remodeling fat body of Drosophila.
