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.
Fox and colleagues report that phosphorylation of profilin-1 in endothelial cells induces HIF-1α activation, leading to tumour angiogenesis in glioblastoma.
Beachy and colleagues use a chemical carcinogenesis mouse model of bladder cancer to demonstrate that an Shh-expressing basal urothelial stem cell is the cell of origin of invasive bladder carcinoma, and to analyse the progression of these lesions.
Connexins localize to the plasma membrane, where they form gap junctions between cells. Cuervo and colleagues report that connexins associate with autophagosome precursor structures in the plasma membrane and inhibit autophagosome biogenesis. Nutrient deprivation relieves this inhibition and promotes autophagic degradation of connexin proteins.
The Cvt pathway in yeast operates constitutively, but the mechanism by which non-cargo material is excluded from the vacuole is incompletely defined. Martens and colleagues show that cargo binding to the cargo receptor Atg19 exposes further Atg8 binding sites on the receptor, which draws the isolation membrane around the autophagic cargo and prevents inclusion of non-cargo material in autophagosomes.
The surface area of neurons increases rapidly during neurite extension. Galli and colleagues show that the endoplasmic reticulum (ER)-resident SNARE protein Sec22b bridges the ER and plasma membrane during this process and contributes to plasma membrane expansion, but does not promote membrane fusion.
Endothelial cells undergo rearrangements during angiogenic sprouting. Gerhardt and colleagues show that the flux in Notch signalling levels in individual cells of sprouting vessels results in differential dynamics of VE-cadherin at junctions to drive functional endothelial cell rearrangements during sprouting. They also find that differential VE-cadherin dynamics are affected in retinopathy and tumour vessels.
Janes and colleagues use organotypic 3D models, transcriptomic analyses, mathematical modelling and in vivo tumour data to show that single cells oscillate between two anticorrelated expression states defined by TGFBR3 and JUND. They show that this signalling circuit is controlled by the engagement of the extracellular matrix, and propose that dynamic changes in gene expression states might underlie breast tumour heterogeneity.
Del Sal and colleagues demonstrate that the YAP and TAZ effectors of the Hippo pathway are under the control of the mevalonate pathway. They show that mutant p53 and SREBP-dependent activation of mevalonate signalling activates YAP and TAZ and promotes tumour formation in mice, a growth phenotype also conserved in Drosophila.
Vale and colleagues report the distinct abilities of different tubulin isotypes and post-translational modifications to regulate different microtubule motors and their properties.
Lecuit and colleagues use Drosophila embryo cellularization as an in vivo model system, as well as in vitro reconstitution assays, to show that septin mutant embryos display defects in actin organization and that septins are able to crosslink, bundle and bend actin filaments into rings.
Hebrok and colleagues use mouse models to demonstrate that loss of the chromatin modifier Brg1 cooperates with oncogenic KRas to form lesions resembling intraductal papillary mucinous neoplasia that progress to pancreatic adenocarcinoma.
How sensory neurons integrate mechanical signals during touch sensation has remained unclear. Using a combination of laser axotomy and FRET imaging to measure force across single cells and molecules, Goodman and colleagues show that the neuronal spectrin cytoskeleton transduces touch sensation in C. elegans.
Silberzan and colleagues demonstrate that local RhoA activity and mechanical forces control the formation of 'migration fingers', cell protrusions involved in the leader-cell-driven collective migration of epithelial cell monolayers.
Screaton and colleagues delineate a pathway involving the AMPK-related Sik2 kinase using mouse models. They show that Sik2-mediated phosphorylation and subsequent degradation of CDK5R1 (p35) by PJA2 is needed for glucose-induced insulin secretion and β-cell functional compensation in models of hyperglycemia and obesity.
Wang, Yang and colleagues delineate a Snail-β-catenin-miR-146a signalling axis that directs a switch from asymmetric to symmetric cell division, resulting in colorectal cancer stem cell expansion.
Ma and colleagues report that in E-cadherin-deficient basal-like breast cancer cells, α-catenin acts as a tumour suppressor by interacting with and stabilizing IκBα, leading to inhibition of NF-κB signalling.
Hair follicle stem cells (HFSCs) regenerate hair in response to Wnt signalling. Fuchs and colleagues use a genome-wide survey to discover that Wnt effectors TCF3, TCF4 and Groucho (TLE) coordinately repress Wnt target genes. They find that although β-catenin is dispensable for HSFC viability and proliferation, it is essential to relieve this repression to initiate hair follicle fate during the hair regeneration cycle.
Mutations in PINK1 cause early-onset Parkinson’s disease. Martins and colleagues find that the expression levels of genes involved in nucleotide metabolism are upregulated in a Drosophila pink1 mutant, and that this affects neuronal mitochondrial DNA synthesis. They find that enhancing nucleotide synthesis through genetics or pharmacological approaches rescues mitochondrial defects associated with PINK1 mutations.
Meiotic chromosome movement is needed for homologue pairing and synapsis. Watanabe and colleagues identify TERB1 as a protein needed for telomere mobility and attachment to the nuclear envelope, and for telomere enrichment of meiotic cohesin.