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Endothelial–vascular smooth muscle cell communication has a critical role in cardiovascular homeostasis and the pathogenesis of atherosclerosis. A study now demonstrates extracellular-vesicle-mediated transfer of the atheroprotective microRNAs miR-143/145 between endothelial and vascular smooth muscle cells, providing compelling evidence that intercellular transport of miRNAs can influence a pathological process, namely atherosclerosis.
In performing its multiple cellular functions, the cytoplasmic dynein motor is subject to complex regulation involving allosteric mechanisms within the dynein complex, as well as numerous extramolecular interactions controlling subcellular targeting and motor activity. Recent work has distinguished high- and low-load regulatory modes for cytoplasmic dynein, which, combined with a diversity of targeting mechanisms, accounts for a very broad range of functions.
Clathrin adaptor proteins are essential for clathrin-coated vesicle biogenesis, yet the mechanisms governing their recruitment and interactions remain incompletely defined. The clathrin adaptors Gga and AP-1 are now shown to be recruited sequentially to the trans-Golgi network in two waves of clathrin coat assembly, coupled by Pik1-mediated phosphatidylinositol-4-phosphate synthesis. These findings reveal mechanistic insights into the functional and regulatory relationships between these clathrin adaptors.
Tumour cells undergo oncogene-regulated metabolic reprogramming that maximizes survival and growth. However, little is known about metabolic interactions between tumour cells and their non-malignant neighbours in the stroma. Bone-marrow-derived stromal cells are now shown to provide cysteine, an essential nutrient that enables leukaemia cells to resist oxidative stress.
Cancer-associated fibroblasts contribute to malignancy by expressing secreted pro-tumorigenic molecules. The microRNA miR-320 is now shown to be a crucial component of a PTEN-controlled tumour-suppressive axis in stromal fibroblasts. Loss of PTEN and miR-320 induces an oncogenic secretome that reprogrammes the tumour microenvironment to promote invasion and angiogenesis.
Ras GTPases are tethered to cellular membranes by a farnesyl lipid that modifies a carboxy-terminal cysteine. One of the ways Ras traffics between membranes is via fluid-phase diffusion, suggesting that a cytosolic chaperone might be needed to shield the farnesyl lipid during transport. PDE6δ is now revealed to be a farnesyl-binding chaperone that facilitates the trafficking and signalling of Ras.
A protocol for efficient differentiation of human pluripotent stem cells into white and brown adipocytes now enables their detailed examination at a cellular and molecular level, facilitating the study of adipocyte dysfunction in a range of metabolic diseases including diabetes, heart disease and obesity.
