On the cover
Endothelial cell–cell junctions containing VE-cadherin (red) are pulled by radial F-actin bundles (blue) as they remodel in response to the vascular permeability factor thrombin. Huveneers et al. reveal that the mechanosensory protein vinculin (green) protects these junctions from opening during the remodeling process.
Image courtesy of Stephan Huveneers.
See page 641.
- PDF Icon PDF LinkTable of Contents
- PDF Icon PDF LinkEditorial Board
In This Issue
People & Ideas
Beyond the cell
Aurora B controls kinetochore–microtubule attachments by inhibiting Ska complex–KMN network interaction
Aurora B phosphorylation antagonizes the interaction between the Ska complex and the KMN network, thereby controlling Ska recruitment to kinetochores and stabilization of kinetochore–microtubule attachments.
Rather than directly impairing 26S proteasomes, misfolded huntingtin may disrupt cellular proteostasis and lead to competition for limited 26S proteasome capacity.
JunB contributes to Id2 repression and the epithelial–mesenchymal transition in response to transforming growth factor–β
JunB helps set in motion the transcriptional program necessary for the epithelial–mesenchymal transition and tissue fibrosis in response to TGF-β.
Drosophila CK1-γ, gilgamesh, controls PCP-mediated morphogenesis through regulation of vesicle trafficking
CK1-γ/gilgamesh spatially limits the planar cell polarity–regulated process of trichome formation in Drosophila through its effect on polarized vesicle recycling.
The PAR-3–aPKC–PAR-6 complex is recruited to primordial cell–cell junctions, in which aPKC phosphorylates JAM-A to promote junctional maturation.
A specialized subset of VE-cadherin adhesions senses cytoskeletal force and recruits Vinculin to control the stability of endothelial cell–cell junctions during their force-dependent remodeling.
Sperm navigate in a chemoattractant gradient by translating changes in intracellular calcium concentration over time into changes in curvature of the swimming path.