Remodelling of mitochondrial function by import of specific lipids at multiple membrane-contact sites.

Organelles form physical and functional contact between each other to exchange information, metabolic intermediates, and signaling molecules. Tethering factors and contact site complexes bring partnering organelles into close spatial proximity to establish membrane contact sites (MCSs), which specialize in unique functions like lipid transport or Ca2+ signaling. Here, we discuss how MCSs form dynamic platforms that are important for lipid metabolism. We provide a perspective on how import of specific lipids from the ER and other organelles may contribute to remodeling of mitochondria during nutrient starvation. We speculate that mitochondrial adaptation is achieved by connecting several compartments into a highly dynamic organelle network. The lipid droplet appears to be a central hub in coordinating the function of these organelle neighborhoods.

A role for endoplasmic reticulum dynamics in the cellular distribution of microtubules.

The dynamic distribution of the microtubule (MT) cytoskeleton is crucial for the shape, motility, and internal organization of eukaryotic cells. However, the basic principles that control the subcellular position of MTs in mammalian interphase cells remain largely unknown. Here we show by a combination of microscopy and computational modeling that the dynamics of the endoplasmic reticulum (ER) plays an important role in distributing MTs in the cell. Specifically, our physics-based model of the ER­MT system reveals that spatial inhomogeneity in the density of ER tubule junctions results in an overall contractile force that acts on MTs and influences their distribution. At steady state, cells rapidly compensate for local variability of ER junction density by dynamic formation, release, and movement of ER junctions across the ER. Perturbation of ER junction tethering and fusion by depleting the ER fusogens called atlastins disrupts the dynamics of junction equilibration, rendering the ER­MT system unstable and causing the formation of MT bundles. Our study points to a mechanical role of ER dynamics in cellular organization and suggests a mechanism by which cells might dynamically regulate MT distribution in, e.g., motile cells or in the formation and maintenance of neuronal axons.