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Stem cell biology has emerged as one of the most exciting areas of basic and biomedical research. This month, we launch a series of specially commissioned articles that discuss recent advances and challenges in this field.
Sander and colleagues discuss recent evidence for and against the roles of stem cells versus the plasticity of mature cell types in response to injury during regeneration of the adult liver and pancreas.
Barker and colleagues review the history and recent developments of organoid cultures derived from pluripotent stem cells and adult epithelia, and discuss how the technology can be used for basic research as well as translational applications.
Transporting epithelia commonly consist of tubes that mediate between the body and its environment. Lumen formation is closely linked to epithelial morphogenesis, but an open question is how luminal symmetry is broken to generate tubes rather than hollow cysts. A report about the biomechanics of intercellular contacts might now provide some answers.
Broken ends of a budding yeast chromosome exhibit increased mobility, presumably to facilitate repair by recombination. A new study reports that increased mobility reflects the untethering of the broken chromosome, triggered by a DNA damage response that phosphorylates the Cep3 kinetochore protein and weakens the association between the centromere and the spindle pole body.
Lecuit and colleagues show that, depending on its interaction partner, the G-protein-coupled receptor Smog regulates myosin II activation in different locations during Drosophila morphogenesis.
DNA resection is the first step of double-strand break repair by homologous recombination. Broderick et al. find that EXD2 plays a key role in this process by acting as an essential cofactor for the MRN complex.
Durocher and colleagues find that in budding yeast, the movement of chromosomes induced by DNA breaks is due to the loss of attachment of kinetochores to spindle pole bodies and of telomeres to the nuclear periphery, and may promote checkpoint arrest.
Receptor-interacting protein kinase 3 (RIPK3) is a key regulator of necroptosis. Seo et al. show that the E3 ligase CHIP mediates ubiquitylation and lysosomal degradation of RIPK3, thus regulating both necrosome formation and necroptosis.
Eichel et al. show that β-arrestin-mediated MAPK activation by GPCRs involves dissociation of β-arrestin from its activating GPCR, and accumulation of β-arrestin in clathrin-coated structures, where it promotes MAPK signalling.
By culturing rat hepatocyte doublets in microwells with controlled ECM environments, Viasnoff and colleagues show that the lumen between the cells extends anisotropically towards regions of lower intercellular tension.
By proteomics analysis of conditioned media from cells with constitutive mTORC1 activity, Yu and colleagues identify IGF binding protein 5 (IGFBP5) as a protein that is induced by mTORC1 through HIF1 and that blocks IGF-1 signalling.
Kornfeld and colleagues identify miRNAs that are dysregulated in brown adipose tissue in mouse models of obesity and ageing, and show that miR-328 targets Bace1 to promote brown adipogenesis.
Boxem and colleagues perform a yeast two-hybrid screen to identify interactions between C. elegans polarity genes, followed by an RNAi screen to identify the functions of interaction pairs in the establishment and maintenance of cell polarity in various tissues.
