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splitGFP Technology Reveals Dose-Dependent ER-Mitochondria Interface Modulation by α-Synuclein A53T and A30P Mutants
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ER-Mitochondria Communication in Cells of the Innate Immune System

Institute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany
German Cancer Consortium (DKTK), Partner Site Frankfurt, 60590 Frankfurt, Germany
Project Group Translational Medicine and Pharmacology TMP, Fraunhofer Institute for Molecular Biology and Applied Ecology, 60596 Frankfurt, Germany
Author to whom correspondence should be addressed.
Cells 2019, 8(9), 1088;
Received: 14 August 2019 / Revised: 11 September 2019 / Accepted: 13 September 2019 / Published: 15 September 2019
In cells the interorganelle communication comprises vesicular and non-vesicular mechanisms. Non-vesicular material transfer predominantly takes place at regions of close organelle apposition termed membrane contact sites and is facilitated by a growing number of specialized proteins. Contacts of the endoplasmic reticulum (ER) and mitochondria are now recognized to be essential for diverse biological processes such as calcium homeostasis, phospholipid biosynthesis, apoptosis, and autophagy. In addition to these universal roles, ER-mitochondria communication serves also cell type-specific functions. In this review, we summarize the current knowledge on ER-mitochondria contacts in cells of the innate immune system, especially in macrophages. We discuss ER- mitochondria communication in the context of macrophage fatty acid metabolism linked to inflammatory and ER stress responses, its roles in apoptotic cell engulfment, activation of the inflammasome, and antiviral defense. View Full-Text
Keywords: endoplasmic reticulum; mitochondria; macrophages; inflammation; lipid metabolism endoplasmic reticulum; mitochondria; macrophages; inflammation; lipid metabolism
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Namgaladze, D.; Khodzhaeva, V.; Brüne, B. ER-Mitochondria Communication in Cells of the Innate Immune System. Cells 2019, 8, 1088.

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