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oai:recercat.cat:2445/1023422025-12-04T22:46:18Zcom_2072_1057col_2072_478825col_2072_478908col_2072_478917

00925njm 22002777a 4500 dc Santabárbara Ruiz, Paula author López Santillán, Mireya author Martínez Rodríguez, Irene author Binagui Casas, Anahí author Pérez, Lidia author Milán, Marco author Corominas, Montserrat (Corominas Guiu) author Serras Rigalt, Florenci author 2016-10-04T10:23:02Z 2016-10-04T10:23:02Z 2015-10-23 2016-10-04T10:23:07Z 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 (ROS) could act as a signaling mechanism as they can trigger pro-inflammatory responses to protect epithelia from environmental insults. Whether ROS emerge from dead cells and what is the genetic response triggered by ROS is pivotal to understand regeneration of Drosophila imaginal discs. We genetically induced cell death in wing imaginal discs, monitored the production of ROS and analyzed the signals required for repair. We found that cell death generates a burst of ROS that propagate to the nearby surviving cells. Propagated ROS 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 JAK/STAT signaling pathway required for regeneration. Our findings demonstrate that this ROS/JNK/p38/Upd 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. Apoptosi Mort cel·lular Larves Regeneració (Biologia) Antioxidants Drosòfila melanogaster Apoptosis Cell death Larvae Regeneration (Biology) Antioxidants Drosophila melanogaster ROS-Induced JNK and p38 Signaling Is Required for Unpaired Cytokine Activation during Drosophila Regeneration