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Stbd1 promotes glycogen clustering during endoplasmic reticulum stress and supports survival of mouse myoblasts.

Authors
  • Lytridou, Andria A1, 2
  • Demetriadou, Anthi1, 2
  • Christou, Melina3, 2
  • Potamiti, Louiza4
  • Mastroyiannopoulos, Nikolas P3, 2
  • Kyriacou, Kyriacos4, 2
  • Phylactou, Leonidas A3, 2
  • Drousiotou, Anthi1, 2
  • Petrou, Petros P5, 2
  • 1 Department of Biochemical Genetics, The Cyprus Institute of Neurology and Genetics, P.O. Box 23462, 1683 Nicosia, Cyprus. , (Cyprus)
  • 2 Cyprus School of Molecular Medicine, P.O. Box 23462, 1683 Nicosia, Cyprus. , (Cyprus)
  • 3 Department of Molecular Genetics, Function and Therapy, The Cyprus Institute of Neurology and Genetics, P.O. Box 23462, 1683 Nicosia, Cyprus. , (Cyprus)
  • 4 Department of Electron Microscopy/Molecular Pathology, The Cyprus Institute of Neurology and Genetics, P.O. Box 23462, 1683 Nicosia, Cyprus. , (Cyprus)
  • 5 Department of Biochemical Genetics, The Cyprus Institute of Neurology and Genetics, P.O. Box 23462, 1683 Nicosia, Cyprus [email protected] , (Cyprus)
Type
Published Article
Journal
Journal of Cell Science
Publisher
The Company of Biologists
Publication Date
Oct 26, 2020
Volume
133
Issue
20
Identifiers
DOI: 10.1242/jcs.244855
PMID: 32958708
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Imbalances in endoplasmic reticulum (ER) homeostasis provoke a condition known as ER stress and activate the unfolded protein response (UPR) pathway, an evolutionarily conserved cell survival mechanism. Here, we show that mouse myoblasts respond to UPR activation by stimulating glycogenesis and the formation of α-amylase-degradable, glycogen-containing ER structures. We demonstrate that the glycogen-binding protein Stbd1 is markedly upregulated through the PERK signalling branch of the UPR pathway and is required for the build-up of glycogen structures in response to ER stress activation. In the absence of ER stress, Stbd1 overexpression is sufficient to induce glycogen clustering but does not stimulate glycogenesis. Glycogen structures induced by ER stress are degraded under conditions of glucose restriction through a process that does not depend on autophagosome-lysosome fusion. Furthermore, we provide evidence that failure to induce glycogen clustering during ER stress is associated with enhanced activation of the apoptotic pathway. Our results reveal a so far unknown response of mouse myoblasts to ER stress and uncover a novel specific function of Stbd1 in this process, which may have physiological implications during myogenic differentiation.This article has an associated First Person interview with the first author of the paper. © 2020. Published by The Company of Biologists Ltd.

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