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Actin is a globular protein that is a major constituent of the cellular cytoskeleton. Actin can exist in monomeric form as G-actin (globular actin) or can form filaments (F-actin, filamentous actin) and mediates multiple cellular functions, including cell migration, contractility and cytokinesis.
Here the authors show that the nucleus undergoes a transient ‘metamorphosis’ within a nuclear–cytoplasmic DNA damage response linked to health and disease. Through this process, the nuclear envelope projects tubules that capture damaged DNA, mediating its repair.
Here the authors perform modelling to reveal that the timescale of actin-VASP interactions plays a critical role in actin ring formation and filament length determines droplet deformation in VASP droplets: predictions from the model were tested against VASP GAB mutant.
Fibroblasts undergo transient activation into myofibroblasts to restore homeostasis to injured tissues. This Review explores the influence of mechanical cues and epigenetic modifications on (myo)fibroblast activation and memory and discusses potential therapeutic prevention of persistent myofibroblast activation in fibrosis.
Focal adhesions are dynamic structures that link the cell to the extracellular matrix. Here, the authors report that focal adhesions contain tropomyosin-decorated actin filaments, and show evidence that suggests specific functions in adhesion dynamics and cell migration.
Completion of cell division requires severing both the microtubules and the plasma membrane that connects daughter cells. Here, the authors show that branched actin regulates ESCRT localization to promote the microtubule cut, which happens before membrane scission.
Despite the constant renewal of their components, cellular actin networks maintain their overall appearance, through a subtle balance of filament assembly and disassembly. This balance is key to the remodelling of cellular architecture. We discuss the significance of in vitro reconstitutions in deciphering the complexity of actin regulation.
The intestinal epithelium serves as a barrier that facilitates interaction between intrinsic and environmental factors. Aging is accompanied by the gradual deterioration of this barrier. We postulate that barrier dysfunction results from defects in epithelial membrane trafficking that exacerbate age-related metabolic imbalances. Herein, we integrate barrier integrity, protein homeostasis, membrane trafficking and intracellular lipid sensing into an age-determining mechanism.
Moore et al. show the role of actin assemblies in regulating the balanced distribution of a healthy mitochondrial network between daughter cells in mitosis.
Stress fibres form a fully integrated meshwork with the submembranous contractile actin cortex that generates and propagates traction forces across the entire cell.
Cancer cells have now been shown to lack rigidity-sensing due to alteration in cytoskeletal sensor proteins, but can be reversed from a transformed to a rigidity-dependent growth state by the sensor proteins, resulting in restoration of contractility and adhesion.
In zebrafish, pioneer axons of the dorsal root ganglia require the release of synaptic-like vesicles to enter the spinal cord, suggesting that synaptic vesicles have a role in circuit formation ahead of synaptogenesis.