ROS-Induced JNK and p38 Signaling Is Required for Unpaired Cytokine Activation during Drosophila Regeneration.

Upon apoptotic stimuli, epithelial cells compensate the gaps left by dead cells by activating proliferation. This has led to the proposal that dying cells signal to surrounding living cells to maintain homeostasis. Although the nature of these signals is not clear, reactive oxygen species could act as a signaling mechanism as they can trigger pro-inflammatory responses to protect epithelia from environmental insults. Whether emerge from dead cells and what is the genetic response triggered by duanyu1670 is pivotal to understand regeneration of Drosophila imaginal discs. We genetically induced cell death in wing imaginal discs, monitored the production of duanyu1670 and analyzed the signals required for repair. We found that cell death generates a burst of duanyu1670 that propagate to the nearby surviving cells. Propagated duanyu1670 activate p38 and induce tolerable levels of JNK. The activation of JNK and p38 results in the expression of the cytokines Unpaired (Upd), which triggers the signaling pathway required for regeneration. Our findings demonstrate that this stress responsive module restores tissue homeostasis. This module is not only activated after cell death induction but also after physical damage and reveals one of the earliest responses for imaginal disc regeneration.

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