Review
MAM (mitochondria-associated membranes) in mammalian cells: Lipids and beyond

https://doi.org/10.1016/j.bbalip.2013.11.014Get rights and content

Highlights

  • Mitochondria-associated membranes (MAM) are part of the endoplasmic reticulum (ER).

  • MAM are reversibly tethered to mitochondria.

  • Import of some lipids into mitochondria occurs via the MAM.

  • MAM regulate calcium homeostasis, mitochondrial function, autophagy and apoptosis.

  • MAM are implicated in neurodegenerative diseases and glucose homeostasis in humans.

Abstract

One mechanism by which communication between the endoplasmic reticulum (ER) and mitochondria is achieved is by close juxtaposition between these organelles via mitochondria-associated membranes (MAM). The MAM consist of a region of the ER that is enriched in several lipid biosynthetic enzyme activities and becomes reversibly tethered to mitochondria. Specific proteins are localized, sometimes transiently, in the MAM. Several of these proteins have been implicated in tethering the MAM to mitochondria. In mammalian cells, formation of these contact sites between MAM and mitochondria appears to be required for key cellular events including the transport of calcium from the ER to mitochondria, the import of phosphatidylserine into mitochondria from the ER for decarboxylation to phosphatidylethanolamine, the formation of autophagosomes, regulation of the morphology, dynamics and functions of mitochondria, and cell survival. This review focuses on the functions proposed for MAM in mediating these events in mammalian cells. In light of the apparent involvement of MAM in multiple fundamental cellular processes, recent studies indicate that impaired contact between MAM and mitochondria might underlie the pathology of several human neurodegenerative diseases, including Alzheimer's disease. Moreover, MAM has been implicated in modulating glucose homeostasis and insulin resistance, as well as in some viral infections.

Introduction

The normal functioning and survival of eukaryotic cells depend on compartmentalization of metabolic processes within specific sub-cellular organelles. This compartmentalization is achieved by restriction of proteins involved in these processes to distinct intracellular organelles. In addition to the spatial separation of metabolic processes in defined organelles, further metabolic compartmentalization occurs within organelles. For example, many proteins are non-uniformly distributed throughout the endoplasmic reticulum (ER). Consequently, the rough ER, which is bound to ribosomes, is morphologically and functionally distinct from the smooth ER which lacks ribosomes. In addition, the “transitional” ER packages proteins for export to the Golgi and subsequently for secretion, whereas another domain of the ER is involved in ER-associated protein degradation, and a different region of the ER is contiguous with the nuclear envelope. Thus, the ER consists of multiple domains that execute specific functions. In mitochondria, metabolic processes are also segregated to distinct sub-compartments so that the outer and inner membranes of mitochondria have distinct lipid and protein compositions and perform different functions. For example, proteins utilized for ATP production via the electron transport chain and oxidative phosphorylation are restricted to mitochondrial inner membranes. Despite this extensive segregation of metabolic processes to and within specific intracellular organelles, inter-organelle communication between the ER and mitochondria is crucial for processes such as lipid synthesis and transport, mitochondrial functions, the regulation of calcium homeostasis and apoptosis. Experimental evidence indicates that one mechanism by which inter-organelle communication is achieved is by close apposition, or transient contact, between membranes of different types of organelle. This review will focus on the membrane contacts that are formed between the ER and mitochondria in mammalian cells. The mechanisms by which these zones of contact participate in key cellular processes such as lipid synthesis, calcium homeostasis, mitochondrial function and survival will be discussed.

Section snippets

Discovery of ER–mitochondria contact sites and mitochondria-associated membranes (MAM)

Over the past 4 decades, numerous ultrastructural/electron microscopic studies have detected regions of close apposition between the ER and mitochondria [1], [2]. However, since these studies provided only morphological data, the reports were frequently dismissed as being artefactual. Nevertheless, subsequent subcellular fractionation studies on rat liver using differential centrifugation have revealed that, indeed, mitochondria can be isolated that are tightly associated with elements of the

Mechanisms of inter-organelle lipid trafficking

Major alterations in the membrane content of most lipids cannot be tolerated by cells or organelles. Consequently, the lipid composition of organelle membranes is tightly regulated. The synthesis of the majority of membrane phospholipids in eukaryotic cells occurs on ER membranes and these lipids are subsequently distributed to other organelles by mechanisms that, for the most part, have remained elusive (reviewed in [41], [42]). Indeed, far more is understood about the molecular mechanisms

Proteins that link the ER to mitochondria

Some key questions regarding the juxtaposition between MAM and mitochondria are: what are the signals that promote the close association between MAM and mitochondrial outer membranes? Does a close proximity between these organelles regulate mitochondrial function? Do specific proteins form tethers that link the ER to mitochondria? If so, what is the molecular nature of these protein tethers? The observation that certain proteins are highly enriched in MAM compared to the bulk of the ER (Table 1

Other functional implications of contact sites between MAM and mitochondria

Within the past decade, several life-and-death functions of cells have been attributed to the formation of MAM-mitochondria contact sites. It is likely that such linkages would provide a means of coordinating the functions of ER and mitochondria. The association between mitochondrial dynamics (fusion and fission) and the tethering of ER to mitochondrial outer membranes was discussed in Section 4. An appropriate balance between mitochondrial fusion and fission is essential for mouse development

Defects in MAM–mitochondria contacts in human disease

A major function of mitochondria is the generation of energy as ATP through oxidative phosphorylation via the electron transport chain. Thus, it is not surprising that mitochondrial dysfunction is a significant component in the etiology of human disorders such as cardiomyopathies, insulin resistance, obesity, cancer and neurodegenerative diseases. Several of these disorders exhibit alterations in mitochondrial morphology and/or calcium homeostasis, both of which can profoundly affect

Summary and conclusions

Although great strides have been made in the past 25 years in understanding the functions of MAM in mammalian cells, many of the studies summarized in Section 6 and Table 2 are clearly still in the initial stages of establishing whether or not defects in MAM contribute to human disease. However, evidence is accumulating in support of the concept that MAM and ER/mitochondria connections are required for many key cellular processes that are involved in life and death events (summarized in Fig. 5).

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