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Goginashvili, Alexander; Zhang, Zhirong; Erbs, Eric; Spiegelhalter, Coralie; Kessler, Pascal; Mihlan, Michael; Pasquier, Adrien; Krupina, Ksenia; Schieber, Nicole; Cinque, Laura; Morvan, Joëlle; Sumara, Izabela; Schwab, Yannick; Settembre, Carmine; Ricci, Romeo

Insulin secretory granules control autophagy in pancreatic β cells

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  • Media type: E-Article
  • Title: Insulin secretory granules control autophagy in pancreatic β cells
  • Contributor: Goginashvili, Alexander; Zhang, Zhirong; Erbs, Eric; Spiegelhalter, Coralie; Kessler, Pascal; Mihlan, Michael; Pasquier, Adrien; Krupina, Ksenia; Schieber, Nicole; Cinque, Laura; Morvan, Joëlle; Sumara, Izabela; Schwab, Yannick; Settembre, Carmine; Ricci, Romeo
  • Published: American Association for the Advancement of Science (AAAS), 2015
  • Published in: Science, 347 (2015) 6224, Seite 878-882
  • Language: English
  • DOI: 10.1126/science.aaa2628
  • ISSN: 0036-8075; 1095-9203
  • Origination:
  • Footnote:
  • Description: Too hungry to eat, too hungry not to eat Pancreatic beta cells, the source of insulin in response to food, employ an unusual mechanism to adapt to nutrient depletion. Goginashvili et al. found that starvation of beta cells induced selective degradation of newly formed insulin granules through their fusion with lysosomes, the cell's garbage disposal units (see the Perspective by Rutter). The nutrient sensor mTOR is recruited to these lysosomes, leading to its local activation and the suppression of autophagy—a process by which cells “eat” their own constituents. Protein kinase D, a major regulator of insulin granule biogenesis, controls this granule degradation in response to nutrient availability. Thus, unlike most other cells, autophagy is not the strategy of choice in beta cells to adapt to starvation. Science , this issue p. 878 ; see also p. 826