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Recruitment of LC3 to damaged Golgi apparatus

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  • معلومة اضافية
    • Contributors:
      Institut Gustave Roussy (IGR); Fudan University; Fudan University [Shanghai]; Rétrovirus endogènes et éléments rétroïdes des eucaryotes supérieurs (UMR 9196); Centre National de la Recherche Scientifique (CNRS)-Institut Gustave Roussy (IGR)-Université Paris-Sud - Paris 11 (UP11); Department of Life Sciences, Imperial College London, London, United Kingdom; Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)); École pratique des hautes études (EPHE); Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU); Département de Structure Subcellulaire et Dynamique Cellulaire [Paris]; Université Paris Dauphine-PSL; Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Curie [Paris]-Centre National de la Recherche Scientifique (CNRS); Rétrovirus endogènes et éléments rétroides des eucaryotes supérieurs (REERES (UMR 8122)); Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Centre National de la Recherche Scientifique (CNRS); École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU); Université Paris Dauphine-PSL-Institut Curie-Centre National de la Recherche Scientifique (CNRS)
    • بيانات النشر:
      HAL CCSD, 2019.
    • الموضوع:
      2019
    • نبذة مختصرة :
      LC3 is a protein that can associate with autophagosomes, autolysosomes, and phagosomes. Here, we show that LC3 can also redistribute toward the damaged Golgi apparatus where it clusters with SQSTM1/p62 and lysosomes. This organelle-specific relocation, which did not involve the generation of double-membraned autophagosomes, could be observed after Golgi damage was induced by various strategies, namely (i) laser-induced localized cellular damage, (ii) local expression of peroxidase and exposure to peroxide and diaminobenzidine, (iii) treatment with the Golgi-tropic photosensitizer redaporfin and light, (iv) or exposure to the Golgi-tropic anticancer peptidomimetic LTX-401. Mechanistic exploration led to the conclusion that both reactive oxygen species-dependent and -independent Golgi damage induces a similar phenotype that depended on ATG5 yet did not depend on phosphatidylinositol-3-kinase catalytic subunit type 3 and Beclin-1. Interestingly, knockout of ATG5 sensitized cells to Golgi damage-induced cell death, suggesting that the pathway culminating in the relocation of LC3 to the damaged Golgi may have a cytoprotective function.
    • ISSN:
      1350-9047
      1476-5403
    • الرقم المعرف:
      10.1038/s41418-018-0221-5⟩
    • Rights:
      OPEN
    • الرقم المعرف:
      edsair.doi.dedup.....0974b8dce2152a8a38041388160aa0fd