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During cell adhesion, integrins are typically thought to require immobilized ligands for spreading. Here, the authors demonstrate that cells can spread and form mature integrin adhesions on fluid substrates by interacting with high-affinity Invasin ligands.

The non-processive motor protein myosin 1b is required for Golgi membrane tubulation. Using a minimal reconstituted system and theoretical analysis, Yamada et al.demonstrate that the mechanism of tubule extraction depends on the catch bond properties of myosin 1b.

Septins are cytoskeletal filaments that localize at constriction sites and impact membrane remodeling. Here authors examine the curvature sensitivity of septins using bilayers on wavy patterns and derive a theoretical model that quantitatively describe the results.

The inverted-BAR domain protein IRSp53 associates with the inner leaflet of tubular membranes such as filopodia. Here, Prévostet al. demonstrate that the I-BAR domain of IRSp53 senses negative membrane curvature, and undergoes phase separation which may aid its clustering upon filopodia generation.

Formation of multivesicular bodies (MVBs) from endosomes or budding of enveloped virus such as HIV-I from the plasma membrane require the ESCRT (endosomal sorting complex required for transport) complexes. An in vitro reconstitution assay unambiguously identifies the function of each ESCRT complex in the sequential events of MVB morphogenesis, from cargo clustering and membrane bud formation to sequestration of cargoes in vesicles, and fission of the vesicles into the lumen of the endosome.

Former evidence suggests a correlation between the function of non-conventional myosin motors and actin dynamics. Here authors use in vitro assays in which they observe that actin sliding on myosin 1b immobilized or bound to a fluid bilayer enhances actin depolymerization at the barbed end.

ESCRT-III complexes assemble in vivo inside membrane structures with a negative Gaussian curvature, but how membrane shape influences ESCRT-III polymerization remains unclear. Here authors use structural and biophysical methods to show how human ESCRT-III polymers assemble on positively curved membranes and induce helical membrane tube formation.

How endocytic pits are formed in clathrin- and caveolin-independent endocytosis remains poorly understood. However, recent insight suggests that different forms of clathrin-independent endocytosis might involve the actin-driven focusing of membrane constituents, the lectin–glycosphingolipid-dependent construction of endocytic nanoenvironments and the use of Bin–Amphiphysin–Rvs (BAR) domain proteins as scaffolding modules.

Holes in endothelial barriers, called transendothelial cell macroapertures (TEMs), are predicted to be limited by line tension of unknown origin. Here the authors identify an actomyosin cable encircling TEMs and establish a role for ezrin in stabilising F-actin bundles, allowing their crosslinking by non-muscle myosin IIa.

Endophilin-A2 (endoA2) is shown to mediate clathrin-independent endocytosis of Shiga and cholera toxins, and to function in parallel with dynamin and actin in the pulling-force-driven scission of Shiga-toxin-induced tubular structures.

HIV particles incorporate host membrane proteins into their envelope to evade the immune system and infect other cells. A study now shows that Gag assembly on the host cell membrane produces a raft-like nanodomain favourable for protein partitioning due to a transbilayer coupling mechanism assisted by long saturated chain lipids and cholesterol.

BIN1/M-Amphiphysin2 is a membrane tubulating protein involved in muscle T-tubule biogenesis and whose loss-of-function is associated with centronuclear myopathies. Picas et al.show that BIN1 enhances the recruitment of its binding partner, dynamin, by clustering PtdIns(4,5)P2 in the plasma membrane.

The cryo-EM structures of ESCRT-III CHMP2A and CHMP3 filaments reveal their mode of polymerization and interaction with negatively curved membrane. VPS4 constricts and cleaves the ESCRT-III CHMP2A–CHMP3 membrane tubes, thus acting as a minimal membrane fission machinery.

A study of endocytosis of Shigella toxin shows that it enters cells via narrow tubular membrane invaginations, with similar properties on cell and model membranes. The toxin induces membrane reorganisation before the formation of tubular invaginations.

Meningococci remodel the plasma membrane of host cells during infection. Here, Charles-Orszag et al. show that plasma membrane remodeling occurs independently of F-actin, along meningococcal type IV pili fibers, by a physical mechanism that they term ‘one-dimensional’ membrane wetting.

Elena Beltrán-Heredia, Feng-Ching Tsai et al. examine the role of cardiolipin in membrane curvature, finding evidence compatible with a model based on membrane elasticity and van der Waals entropy. These results promote understanding of the interplay between membrane curvature and composition.

The N-BAR domain protein BIN1 acts as a scaffolding protein during filopodia formation in myoblast cells, together with identified co-factors.