Journal
CELL DEATH AND DIFFERENTIATION
Volume 26, Issue 8, Pages 1467-1484Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41418-018-0221-5
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Funding
- Portuguese Science Foundation [SFRH/BPD/93562/2013]
- Ligue contre le Cancer (equipe labelisee)
- Agence National de la Recherche (ANR)Projets blancs
- ANR
- Association pour la recherche sur le cancer (ARC)
- Canceropole Ile-de-France
- Institut National du Cancer (INCa)
- Institut Universitaire de France
- Fondation pour la Recherche Medicale [FDM20140630126, FDM 40739]
- European Commission (ArtForce)
- European Research Council (ERC)
- LeDucq Foundation
- LabEx Immuno-Oncology
- RHU Torino Lumiere
- SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE)
- SIRIC Cancer Research and Personalized Medicine (CARPEM)
- Paris Alliance of Cancer Research Institutes (PACRI)
- Centre National de la Recherche Scientifique (CNRS)
- Institut Curie
- LabEx CelTisPhyBio (IDEX PSL) [ANR10-IDEX-0001-02, ANR-10-LBX-0038]
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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 SQSTMl/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.
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