dc.creator | Ingaramo, María Clara | |
dc.creator | Sánchez, Juan Andrés | |
dc.creator | Perrimon, Norbert | |
dc.creator | Dekanty, Andres | |
dc.date.accessioned | 2021-10-28T14:29:44Z | |
dc.date.accessioned | 2022-10-15T08:26:06Z | |
dc.date.available | 2021-10-28T14:29:44Z | |
dc.date.available | 2022-10-15T08:26:06Z | |
dc.date.created | 2021-10-28T14:29:44Z | |
dc.date.issued | 2020-10 | |
dc.identifier | Ingaramo, María Clara; Sánchez, Juan Andrés; Perrimon, Norbert; Dekanty, Andres; Fat Body p53 Regulates Systemic Insulin Signaling and Autophagy under Nutrient Stress via Drosophila Upd2 Repression; Elsevier; Cell Reports; 33; 4; 10-2020; 1-30 | |
dc.identifier | 2211-1247 | |
dc.identifier | http://hdl.handle.net/11336/145325 | |
dc.identifier | CONICET Digital | |
dc.identifier | CONICET | |
dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/4364913 | |
dc.description.abstract | The tumor suppressor p53 regulates multiple metabolic pathways at the cellular level. However, its role in the context of a whole animal response to metabolic stress is poorly understood. Using Drosophila, we show that AMP-activated protein kinase (AMPK)-dependent Dmp53 activation is critical for sensing nutrient stress, maintaining metabolic homeostasis, and extending organismal survival. Under both nutrient deprivation and high-sugar diet, Dmp53 activation in the fat body represses expression of the Drosophila Leptin analog, Unpaired-2 (Upd2), which remotely controls Dilp2 secretion in insulin-producing cells. In starved Dmp53-depleted animals, elevated Upd2 expression in adipose cells and activation of Upd2 receptor Domeless in the brain result in sustained Dilp2 circulating levels and impaired autophagy induction at a systemic level, thereby reducing nutrient stress survival. These findings demonstrate an essential role for the AMPK-Dmp53 axis in nutrient stress responses and expand the concept that adipose tissue acts as a sensing organ that orchestrates systemic adaptation to nutrient status. | |
dc.language | eng | |
dc.publisher | Elsevier | |
dc.relation | info:eu-repo/semantics/altIdentifier/url/https://linkinghub.elsevier.com/retrieve/pii/S2211124720313103 | |
dc.relation | info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.celrep.2020.108321 | |
dc.rights | https://creativecommons.org/licenses/by-nc-nd/2.5/ar/ | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | AMPK | |
dc.subject | DROSOPHILA | |
dc.subject | FAT BODY | |
dc.subject | INSULIN-PRODUCING CELLS | |
dc.subject | INTER-ORGAN COMMUNICATION | |
dc.subject | LEPTIN | |
dc.subject | METABOLISM | |
dc.subject | P53 | |
dc.subject | STARVATION | |
dc.subject | UPD2 | |
dc.title | Fat Body p53 Regulates Systemic Insulin Signaling and Autophagy under Nutrient Stress via Drosophila Upd2 Repression | |
dc.type | info:eu-repo/semantics/article | |
dc.type | info:ar-repo/semantics/artículo | |
dc.type | info:eu-repo/semantics/publishedVersion | |