期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 110, 期 40, 页码 16003-16008出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1315784110
关键词
mitochondrial dynamics; live cell imaging; actin
资金
- 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
- Fondation pour la Recherche Medicale
- Intramural Research Program of the National Institutes of Neurological Disorders and Stroke
- National Institutes of Health
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.
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