Lipid Metabolism at Membrane Contacts: Dynamics and Functions Beyond Lipid Homeostasis.

Jiesi Xu,Xun Huang

doi:10.3389/fcell.2020.615856

Abstract

Membrane contact sites (MCSs), regions where the membranes of two organelles are closely apposed, play critical roles in inter-organelle communication, such as lipid trafficking, intracellular signaling, and organelle biogenesis and division. First identified as “fraction X” in the early 90s, MCSs are now widely recognized to facilitate local lipid synthesis and inter-organelle lipid transfer, which are important for maintaining cellular lipid homeostasis. In this review, we discuss lipid metabolism and related cellular and physiological functions in MCSs. We start with the characteristics of lipid synthesis and breakdown at MCSs. Then we focus on proteins involved in lipid synthesis and turnover at these sites. Lastly, we summarize the cellular function of lipid metabolism at MCSs beyond mere lipid homeostasis, including the physiological meaning and relevance of MCSs regarding systemic lipid metabolism. This article is part of an article collection entitled: Coupling and Uncoupling: Dynamic Control of Membrane Contacts.

Highlights

Compartmentalization is a basic organizational principle of cells
Membrane contact sites permit the speed and spatial confinement that are required for the intricate control of cellular processes and organelle biogenesis
It has been observed that Membrane contact sites (MCSs) are resistant to harsh separation methods, probably because of the biophysical properties of their resident membrane proteins and lipids

Summary

Introduction

Compartmentalization is a basic organizational principle of cells. It can be achieved by intracellular membranes, which act as physical barriers to optimize the efficiency of cellular processes that occur within organelles (Aguzzi and Altmeyer, 2016). The association of PI4P with Osh3 facilitates the interaction between ORD, a lipid transfer domain in Osh3, and the downstream target protein Sac1, stimulating Sac1 PI phosphatase activity (Stefan et al, 2011; Figure 2D).

Results

Conclusion