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Organ and vessel-type-specific differences in endothelial cell barrier composition and properties uncover the distinct importance of the major tight junction protein Claudin5 in restricting agonist-induced leakage.

A critical analysis of recent single-cell transcriptomic studies of Drosophila blood cells confirms the extreme plasticity of the major phagocyte class, identifies a new class of blood cell, and suggests relationships to blood cells in other insects.

Single-cell RNA-sequencing, spatial genomics, and histological analyses reveal that cold-induced brown adipose neogenesis is a complex adaptive response to elevated metabolic demand involving dynamic interactions between recruited immune cells and a subpopulation of poised adipocyte progenitors.

DIP2 is a conserved protein across fungi and animals that regulates specific diacylglycerol pools by diverting them to storage lipid biosynthesis to enable cellular homeostasis and adaptations.

Clathrin-coated vesicles can be made to form on intracellular membranes using a minimal molecular system, which defines the core vesicle budding machinery.

The ability of Vaccinia virus to induce actin polymerisation depends on the relative binding position of adaptors within the signalling network activating the Arp2/3 complex.

An actin-based Brownian Ratchet enables branched actin networks to generate pushing forces, while a capping protein-based Brownian Ratchet provides force feedback that enables these networks to adapt their architecture in response to changing loads.

Yap interacts with Rif1, a major DNA replication timing factor, and functions as a brake to control the DNA replication program in Xenopus early embryos and post-embryonic stem cells.

Experiments using purified proteins reveal how the network of filaments that underlie cell movement becomes denser when pushing against a stronger mechanical force.

Transcriptomic and bionergetic analysis shows the importance of HIF-1α activation in enabling tissue-resident alveolar macrophages to perform glycolytic metabolism, which prevents their death and attenuates influenza A virus-induced acute lung injury.