Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Macrophages facilitate tumour progression, but it is unclear whether this capability is influenced by tumour-initiating cells. Glioblastoma stem cells are now shown to secrete periostin, a matrix protein that recruits protumoral macrophages and enhances glioblastoma progression in mice.
The protrusion of cilia into extracellular space provides cells with sensors of localized environmental cues that include fluid flow, mechanical force and important growth factors such as Hedgehog. Live imaging has now captured the initial appearance of cilia during embryogenesis, and defined lineage-specific determinants that restrict extra-embryonal ciliogenesis.
Anderson and colleagues report that, although mouse embryonic tissues form primary cilia, in cells destined for extraembryonic lineages, the activities of aurora kinase A and the tubulin deacetylase HDAC6 inhibit ciliogenesis.
Ding and colleagues report that blood platelets recruited to the lung by injury release the chemokine SDF-1, which interacts with its receptor CXCR4 on pulmonary capillary endothelial cells and thereby initiates alveolar regeneration.
Elliott et al. use high-resolution imaging, microfabrication and computational analyses to show that the interplay between cell-surface curvature and activity and cortical recruitment of myosin II, control cell migration in 3D matrices.
Hyman, Muller and colleagues characterize how mitotic rounding forces relate to the dynamics of the actomyosin cortex. They find that myosin II enables the cell to resist deformation.
Cunningham et al. characterize the ubiquitin chain linkages regulated by the opposing activities of the E3 ligase parkin and the deubiquitylation enzyme USP30 on mitochondria.
Bao and colleagues report that glioblastoma cancer stem cells produce periostin, which in turn recruits tumour-associated macrophages to the tumour site to foster growth.
Wang and colleagues report that cancer-cell-derived extracellular vesicles that contain miR-122 reprogram glucose metabolism of premetastatic niche cells to alter nutrient availability and promote metastasis.
