Membrane trafficking articles from across Nature Portfolio

The plasma membrane of eukaryotic cells can fold inwards to create reservoirs that store or release excess membrane. Zhu et al. show that Salmonella-secreted effectors modulate these reservoirs to facilitate host cell invasion.

The mechanisms transporting fatty acids into the cell are not completely understood. Here, the authors discover a selective transporter for a specific class of lipids, and show its role in regulating neutrophil function during myocardial ischemia-reperfusion injury.

Growth factors rapidly raise cellular glycolysis. Here, authors unveil a mechanism where RTK/GLUT1-containing endocytic vesicles deliver glucose to glycolytic enzymes near mitochondria without upregulating cell surface glucose transporters.

Suda and colleagues explore the enduring consequences of plasma membrane injury in budding yeast and mammalian cells. Their findings highlight that membrane damage induces irreversible cell-cycle arrest and premature cellular senescence, whereas upregulation of plasma membrane repair suppresses them.

The generation of clathrin-coated vesicles during endocytosis requires the co-ordinated recruitment of dozens of proteins to the plasma membrane. We discovered that the plant TPLATE (or TSET) complex (TPC) undergoes biomolecular condensation through interactions with plasma membrane phospholipids and, via weak multivalent interactions, recruits clathrin and other endocytic proteins to facilitate the efficient progression of endocytosis.

Despite a growing understanding of the immunostimulatory properties of mitochondrial DNA (mtDNA), little is known about how and why mtDNA escapes its mitochondrial confines. A study now describes an endosomal trafficking pathway that facilitates mtDNA egress and provides an additional mechanism of mtDNA release in vitro.

How do metabolic stresses trigger catabolic autophagy for cell survival? A study now reveals that the metabolite sensor Pho81 integrates into and activates the kinase activity of the Atg1 complex for pexophagy triggered by phosphate starvation. This demonstrates the plasticity of the autophagy-initiating Atg1 complex.