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.
MicroRNAs regulate cancer metastasis by modulating both the intrinsic properties of tumour cells and their interactions with the tumour stroma. Both strands of the miR-126/miR-126* duplex are now shown to simultaneously target the Sdf-1α cytokine to reduce the recruitment of mesenchymal stem cells and inflammatory monocytes to primary tumours, thereby inhibiting lung metastasis.
Endocytosis has proved to be a versatile mechanism regulating diverse cellular processes, ranging from nutrient uptake to intracellular signal transduction. New work reinforces the importance of endocytosis for VEGF receptor signalling and angiogenesis in the developing eye, and describes a mechanism for its differential regulation in angiogenic versus quiescent endothelial cells.
Centrosomes play an important role in Drosophila melanogaster stem cells, where the different size and activity of the two centrosomes help these cells divide asymmetrically. The molecular basis of the centrosome asymmetry has remained unclear, but new work highlights the centrosomal protein Centrobin as a key player in this process.
α-catenin exists as part of the cadherin–catenin adhesion complex as well as in a cytoplasmic pool. However, which of these pools is responsible for its biological impact remains controversial. A structure-function analysis in Drosophila melanogaster illuminates how the molecular properties of α-catenin translate into functional outcomes in an intact organism.
In Drosophila neuroblasts, Centrobin marks the daughter centriole, which, in contrast to the mother centriole, is able to retain pericentriolar material (PCM) and organize an interphase microtubule aster thought to guide the subsequent asymmetric division. Gonzalez and colleagues demonstrate that Centrobin is necessary and sufficient to mediate this centrosome asymmetry, that it binds centriole and PCM proteins, and is regulated by POLO kinase.
The sprouting activity of filopodia emerging from endothelial sprouting cells needs to be compensated for in mature stable vessels. Adams and colleagues find that sprouting cells in mouse retinal vasculature show high VEGF uptake and VEGF receptor turnover, both essential for sprouting. These are inhibited by an aPKC-mediated decrease in VEGF receptor endocytosis in mature vessels, through a mechanism implicating clathrin-associated proteins, the transmembrane protein ephrin-B2 and the polarity factor PAR-3.
Tepass and colleagues use a series of mutant α-catenin forms to study the role of this protein in Drosophilain vivo. Their data support a model in which monomeric α-catenin links the cadherin–β-catenin complex at adherens junction to the actin cytoskeleton.
Shen and colleagues find that initiation of prostate tumours by basal or luminal epithelial cells in mice leads to distinct tumour signatures. Interestingly, they find that although oncogenic transformation of basal cells gives rise to tumours with luminal phenotypes, tumours of luminal origins are more aggressive in functional tests and the distinct signature correlated with that of patients with aggressive tumours.
Wang and colleagues show that miR-126 and miR-126* suppress metastasis by inhibiting the production of the Sdf-1α cytokine in mouse mammary tumours, resulting in decreased recruitment of mesenchymal stem cells and inflammatory monocytes to the tumour stroma.
Oct4 cannot be replaced by other members of the same family of transcription factors to induce reprogramming. By comparing the structure of the POU family domain of Oct4 complexed to DNA with that of others, Schöler and colleagues identify an α-helix that is exposed on the surface of Oct4 and provides an interaction platform to recruit epigenetic modifiers to Oct4 targets. Mutations abolishing this helix suppress the reprogramming properties of Oct4.
Adipocytes have been suggested to arise from prospective progenitors of endothelial or haematopoietic origin. Rödeheffer and colleagues use lineage tracing to rule out that this is the case for white adipocytes, and show that they instead arise from CD24+ cells that are characterized by the expression of PdgfR (platelet-derived growth factor receptor).
Van den Brink and colleagues show that Nrf2, a regulator of the oxidative stress response, is required for several aspects of haematopoietic stem cell maintenance. Loss of Nrf2 results in the hyper-proliferation of haematopoietic stem and progenitor cells (HSPCs). Nrf2 is also required for HSPC migration and retention to their niche.
Emery and colleagues show that during collective migration of Drosophila border cells, the Rab11 small GTPase regulates Rac activity throughout the cell cluster. They propose that Rab11 activates the actin-binding protein Moesin at the cell cortex, which allows the spatial restriction of Rac activity to the leading cell of the group.
Maliga and colleagues have produced a library of bacterial artificial chromosome (BAC) transgenes encoding tagged human kinesin and myosin motors, and have generated a collection of BAC-expressing human and mouse cell lines for the study of motor function.
