Fiche publication
Date publication
février 2015
Auteurs
Membres identifiés du Cancéropôle Est :
Dr SUMARA Izabela
Tous les auteurs :
Goginashvili A, Zhang Z, Erbs E, Spiegelhalter C, Kessler P, Mihlan M, Pasquier A, Krupina K, Schieber N, Cinque L, Morvan J, Sumara I, Schwab Y, Settembre C, Ricci R
Lien Pubmed
Résumé
Pancreatic beta cells lower insulin release in response to nutrient depletion. The question of whether starved beta cells induce macroautophagy, a predominant mechanism maintaining energy homeostasis, remains poorly explored. We found that, in contrast to many mammalian cells, macroautophagy in pancreatic beta cells was suppressed upon starvation. Instead, starved beta cells induced lysosomal degradation of nascent secretory insulin granules, which was controlled by protein kinase D (PKD), a key player in secretory granule biogenesis. Starvation-induced nascent granule degradation triggered lysosomal recruitment and activation of mechanistic target of rapamycin that suppressed macroautophagy. Switching from macroautophagy to insulin granule degradation was important to keep insulin secretion low upon fasting. Thus, beta cells use a PKD-dependent mechanism to adapt to nutrient availability and couple autophagy flux to secretory function.
Référence
Science. 2015 Feb 20;347(6224):878-82
