Atypical mitochondrial fission upon bacterial infection
Autor: | Richard J. Youle, Amy E. Palmer, Fabrizia Stavru, Pascale Cossart, Chunxin Wang |
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Přispěvatelé: | Institut National de la Recherche Agronomique (INRA), Interactions Bactéries-Cellules (UIBC), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), University of Colorado [Boulder], National Institutes of Health [Bethesda] (NIH), Institut Pasteur Institut National de la Sant [604], Institut National de la Recherche Agronomique Unit, Nationale pour la Recherche, postdoctoral fellowships from European Molecular Biology Organization, recherche Medicale, Intramural Research Program of the National Institutes of Neurological Disorders and Stroke, National Institutes of Health, ProdInra, Migration, Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), National Institute of Neurological Disorders and Stroke, echerche Medicale |
Jazyk: | angličtina |
Rok vydání: | 2013 |
Předmět: |
[SDV]Life Sciences [q-bio]
Fluorescent Antibody Technique Mitochondrion MESH: Heat-Shock Proteins Endoplasmic Reticulum MESH: Listeria monocytogenes GTP Phosphohydrolases Hemolysin Proteins 0302 clinical medicine FUSION MAMMALIAN-CELLS Staurosporine Listeriosis LISTERIA-MONOCYTOGENES MESH: Fluorescent Antibody Technique Heat-Shock Proteins 0303 health sciences Multidisciplinary MESH: Real-Time Polymerase Chain Reaction Listeriolysin O PROTEIN HFIS1 MESH: Mitochondrial Proteins Biological Sciences Cell biology APOPTOSIS [SDV] Life Sciences [q-bio] MESH: Hemolysin Proteins Mitochondrial fission Microtubule-Associated Proteins actin medicine.drug Dynamins endocrine system MESH: GTP Phosphohydrolases Bacterial Toxins Blotting Western ENDOPLASMIC-RETICULUM DRP1 Biology Real-Time Polymerase Chain Reaction Mitochondrial Proteins 03 medical and health sciences MESH: Endoplasmic Reticulum medicine Humans MESH: Blotting Western Fragmentation (cell biology) PROTEOLYTIC CLEAVAGE 030304 developmental biology MESH: Humans Endoplasmic reticulum Listeria monocytogenes Molecular biology Fusion protein mitochondrial dynamics MESH: Mitochondrial Dynamics MESH: Dynamins live cell imaging MESH: Microtubule-Associated Proteins MESH: Bacterial Toxins MESH: Listeriosis MESH: HeLa Cells DNAJA3 MORPHOLOGY OUTER-MEMBRANE 030217 neurology & neurosurgery HeLa Cells |
Zdroj: | Proceedings of the National Academy of Sciences of the United States of America Proceedings of the National Academy of Sciences of the United States of America, 2013, 110 (40), pp.16003-16008. ⟨10.1073/pnas.1315784110⟩ Proceedings of the National Academy of Sciences of the United States of America, National Academy of Sciences, 2013, 110 (40), pp.16003-16008. ⟨10.1073/pnas.1315784110⟩ Proceedings of the National Academy of Sciences |
ISSN: | 0027-8424 1091-6490 |
DOI: | 10.1073/pnas.1315784110⟩ |
Popis: | International audience; We recently showed that infection by Listeria monocytogenes causes mitochondrial network fragmentation through the secreted pore-forming toxin listeriolysin O (LLO). Here, we examine factors involved in canonical fusion and fission. Strikingly, LLOinduced mitochondrial fragmentation does not require the traditional fission machinery, as Drp1 oligomers are absent from fragmented mitochondria following Listeria infection or LLO treatment, as the dynamin-like protein 1 (Drp1) receptor Mff is rapidly degraded, and as fragmentation proceeds efficiently in cells with impaired Drp1 function. LLO does not cause processing of the fusion protein optic atrophy protein 1 (Opa1), despite inducing a decrease in the mitochondrial membrane potential, suggesting a unique Drp1-and Opa1-independent fission mechanism distinct from that triggered by uncouplers or the apoptosis inducer staurosporine. We show that the ER marks LLO-induced mitochondrial fragmentation sites even in the absence of functional Drp1, demonstrating that the ER activity in regulating mitochondrial fission can be induced by exogenous agents and that the ER appears to regulate fission by a mechanism independent of the canonical mitochondrial fission machinery. |
Databáze: | OpenAIRE |
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