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Tumour cells are influenced by their microenvironment, which can promote uncontrolled growth, invasion and metastasis. The GATA3 transcription factor is now shown to regulate the tumour microenvironment by inducing the expression of miR-29b in cancer cells. This microRNA in turn inhibits the expression of genes involved in angiogenesis and extracellular matrix signalling and remodelling to suppress metastasis.
Most organs are composed of tubes of differing cellular architectures, including intracellular 'seamless' tubes. Two studies examining the morphogenesis of the seamless tubes formed by the excretory canal cell in Caenorhabditis elegans reveal a previously unappreciated role for osmoregulation of tubulogenesis: hyperosmotic shock recruits canalicular vesicles to the lumenal membrane to promote seamless tube growth.
Werb and colleagues demonstrate that GATA3, a transcription factor that promotes luminal differentiation in the mammary gland, suppresses breast cancer metastasis to the lung by upregulating miR-29b. This microRNA suppresses pro-metastatic characteristics, including mesenchymal traits and the expression of microenvironmental factors involved in angiogenesis and extracellular matrix remodelling.
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.
Cédric Blanpain discusses the progress achieved in identifying and characterizing the cellular origins of different solid tumours in mouse models of skin, brain, breast, gut and lung cancer, using genetic lineage tracing approaches.
Gobel and colleagues show that the cortical protein ERM-1 drives expansion of the unicellular tube that constitutes the Caenorhabditis elegans excretory canal by recruiting membrane and cytoskeletal components, and the water channel aquaporin, to the apical side of the tube.
Arlotta and Rouaux show that expression of the transcription factor Fezf2 in vivo is sufficient to redirect post-mitotic callosal projection neurons from one particular layer of the brain to corticofugal projection neurons that pertain to a different layer, including a redirection of their axonal connectivity.
Labouesse and colleagues examine the steps of excretory canal growth in nematodes. They delineate the importance of osmoregulated vesicle fusion with the lumen, and of a subapical cytoskeletal web to ensure straight lumen growth. They identify PROS-1 as a transcription factor essential for lumen growth through modulation of the osmosensitive kinase GCK-3 and intermediate filament protein IFB-1.
Cortical actin is implicated in cell shape regulation during mitosis. Melchior and colleagues reveal that SCFFbxw5-mediated ubiquitylation and degradation of the actin remodeller Eps8 is required for timely cell rounding and progression into metaphase, whereas the capping activity of Eps8 is needed for mitotic exit.
Xenopus laevis and tropicalis tadpoles display incredible regenerative capacity of their tail. Amaya and colleagues find that tadpole tail amputation induces the production of reactive oxygen species (ROS) to induce cell proliferation and regeneration, through activation of the Wnt/β-catenin and Fgf20 signalling pathways.
Muller and Vousden discuss the functional outcomes of mutant p53 in cancer and outline the mechanisms through which gain-of-function mutant p53 forms exert their oncogenic effects.
