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Notch and VEGF signalling controls the specification of endothelial cells to tip and stalk cells during angiogenesis sprouting. Alitalo and colleagues show that macrophage-derived VEGF-C activates VEGFR2 to contribute to the conversion of endothelial cells from a tip- to a stalk-cell fate when two sprouts fuse to ensure vessel growth and branching.
Doxsey and colleagues report that midbodies accumulate in stem cells, including induced pluripotent stem cells and potential cancer-initiating cells. Loss of midbodies accompanies stem-cell differentiation and is mediated through binding of the autophagy receptor NBR1 to the midbody protein CEP55. Downregulation of NBR1 is associated with enrichment of midbodies, enhanced reprogramming and increased tumorigenicity in cancer cells.
Overlapping antiparallel microtubules are important in cellular structures such as the mitotic spindle. Diez and colleagues use an in vitro system and mathematical modelling to show that the formation of stable overlaps involves a motor such as kinesin-14, which slides microtubules apart, and a passive microtubule crosslinker, Ase1, which accumulates at microtubule overlapping regions and slows microtubule sliding to prevent their separation.
Here, we make a case for multivariate measurements in cell biology with minimal perturbation. We discuss how correlative data can identify cause-effect relationships in cellular pathways with potentially greater accuracy than conventional perturbation studies.
A precise role for the canonical Wnt pathway in maintaining pluripotency in mouse embryonic stem cells (mESCs) has been debated. Four recent reports add pieces to the puzzle and together these results may help establish a robust model.
The mitochondrial network fragments during mitosis to allow proper segregation of the organelles between daughter cells. Two mitotic kinases, the cyclin B–CDK1 complex and Aurora A, are now shown to cooperate with the small G protein RALA and its effector RALBP1 to promote DRP1 phosphorylation and mitochondrial fission.
The microtubules that attach kinetochores to chromosomes (K-fibres) are stabilized in prometaphase to allow for accurate chromosome segregation. Kapoor and colleagues find that the B56-PP2A phosphatase stabilizes K-fibres potentially by counteracting the phosphorylation of kinetochore substrates that is mediated by Aurora B and Plk1.
Mammalian oocyte maturation involves two asymmetric meiotic divisions that require the positioning of the meiotic spindle near the cortical area from which the extrusion of the polar bodies occurs. Li and colleagues show that the nucleating activity of the Arp2/3 complex, localized at the cortical actin cap, induces actin-filament flow away from the complex, creating a cytoplasmic streaming that pushes the spindle towards the cortex.
Franzoso and colleagues show that NF-κB protects cells from nutrient-starvation-induced necrosis by upregulating mitochondrial respiration through increased p53-dependent expression of the SCO2 enzyme. Conversely, inhibition of NF-κB results in increased aerobic glycolysis, known as the Warburg effect, thus promoting oncogenic transformation, and affects metabolic adaptation during tumorigenesis in vivo.
The LIN-5/NuMA pathway is needed to correctly position the mitotic spindle for asymmetric division. Now van den Heuvel and colleagues find that polarity kinase aPKC–PKC-3 phosphorylates LIN-5 to direct the localization of the spindle in the early embryos of Caenorhabditis elegans.
Drosophila L(3)mbt mutant brains are shown to develop brain tumours owing to derepression of the target genes of the Salvador–Warts–Hippo pathway, resulting in overproliferation of neuroepithelial cells in the optic lobes. L(3)mbt is found to act in this process by binding to insulator elements at the promoters of these target genes.
Cancer stem cells (CSCs) have been linked to the maintenance and progression of several tumours, but the properties of human CSCs are not well known. Reprogramming of human somatic cells during neoplastic in vitro transformation is shown to confer the properties of stem cells to primary differentiated fibroblasts. The cells that give rise to tumours in this case express the SSEA-1 antigen.
Unpaired morphogen specifies migratory border-cell migration in a STAT-dependent manner, so that cells with low STAT signalling do not migrate. In a feedback loop, miR-279 generates a cell-fate threshold in STAT signalling in response to the Upd gradient to prevent inappropriate migration.