The endoplasmic reticulum–mitochondria connection: One touch, multiple functions

Abstract

The endoplasmic reticulum (ER) and mitochondria are tubular organelles with a characteristic "network structure" that facilitates the formation of interorganellar connections. The ER and mitochondria join together at multiple contact sites to form specific domains, termed mitochondria-ER associated membranes (MAMs), with distinct biochemical properties and a characteristic set of proteins. The functions of these two organelles are coordinated and executed at the ER-mitochondria interface, which provides a platform for the regulation of different processes. The roles played by the ER-mitochondria interface range from the coordination of calcium transfer to the regulation of mitochondrial fission and inflammasome formation as well as the provision of membranes for autophagy. The novel and unconventional processes that occur at the ER-mitochondria interface demonstrate its multifunctional and intrinsically dynamic nature. This article is part of a Special Issue entitled: Dynamic and ultrastructure of bioenergetic membranes and their components.

ER-stress mobilization of death-associated protein kinase-1–dependent xenophagy counteracts mitochondria stress–induced epithelial barrier dysfunction

“…Mitochondria couple with the endoplasmic reticulum (ER), where reactive oxygen species (ROS) are important in protein folding (16). When improperly folded proteins accumulate in the ER, an ER stress program (or unfolded protein response (UPR)) occurs.…”

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Tumor suppressive Ca2+ signaling is driven by IP3 receptor fitness

“…Alterations in the expression, activity and regulation of Ca 2+ -transport systems both at the plasma membrane and at organelles like the endoplasmic reticulum (ER) and mitochondria have been implicated in oncogenesis and neoplasia [1,4]. These changes result in aberrant Ca 2+ -signaling events that could favor resistance to cell death, migration or senescence escape [5].Over the last decade, we learnt that tight contacts and functional connections involving Ca 2+ exchanges between the ER, the main intracellular Ca 2+ -storage organelle, and the mitochondria are pivotal for cell-fate decisions [3,[6][7][8].These contact sites contain chaperone-coupled Ca 2+ -flux systems: the IP 3 receptors (IP 3 Rs) at the ER side and the voltage-dependent anion channels (VDACs) at the mitochondrial outer membrane side [9]. These are controlled/exploited by several cellular factors and regulatory proteins, including oncogenes and tumor suppressors [10][11][12].…”