There is now growing evidence of the emergence and biological functionality of liquid crystal features, including nematic order and topological defects, in cellular tissues. However, how such features that intrinsically rely on particle elongation, emerge in monolayers of cells with isotropic shapes is an outstanding question. In this article we present a minimal model of cellular monolayers based on cell deformation and force transmission at the cell-cell interface that explains the formation of topological defects and captures the flow-field and stress patterns around them. By including mechanical properties at the individual cell level, we further show that the instability that drives the formation of topological defects and leads to active turbulence, emerges from a feedback between shape deformation and active driving. The model allows us to suggest new explanations for experimental observations in tissue mechanics, and to propose designs for future experiments. arXiv:1811.05040v2 [cond-mat.soft]

Actomyosin machinery endows cells with contractility at a single cell level. However, within a monolayer, cells can be contractile or extensile based on the direction of pushing or pulling forces exerted by their neighbours or on the substrate. It has been shown that a monolayer of fibroblasts behaves as a contractile system while epithelial or neural progentior monolayers behave as an extensile system. Through a combination of cell culture experiments and in silico modeling, we reveal the mechanism behind this switch in extensile to contractile as the weakening of intercellular contacts. This switch promotes the buildup of tension at the cell-substrate interface through an increase in actin stress fibers and traction forces. This is accompanied by mechanotransductive changes in vinculin and YAP activation. We further show that contractile and extensile differences in cell activity sort cells in mixtures, uncovering a generic mechanism for pattern formation during cell competition, and morphogenesis.

Morphological changes during development, tissue repair, and disease largely rely on coordinated cell movements and are controlled by the tissue environment. Epithelial cell sheets are often subjected to large-scale deformation during tissue formation. The active mechanical environment in which epithelial cells operate have the ability to promote collective oscillations, but how these cellular movements are generated and relate to collective migration remains unclear. Here, combining in vitro experiments and computational modeling, we describe a form of collective oscillations in confined epithelial tissues in which the oscillatory motion is the dominant contribution to the cellular movements. We show that epithelial cells exhibit large-scale coherent oscillations when constrained within micropatterns of varying shapes and sizes and that their period and amplitude are set by the smallest confinement dimension. Using molecular perturbations, we then demonstrate that force transmission at cell-cell junctions and its coupling to cell polarity are pivotal for the generation of these collective movements. We find that the resulting tissue deformations are sufficient to trigger osillatory mechanotransduction of YAP within cells, potentially affecting a wide range of cellular processes.

The fully differential computation of the hadronic production cross section of a Higgs boson via bottom quarks is presented at NNLO in QCD. Several differential distributions with their corresponding scale uncertainties are presented for the 8 TeV LHC. This is the first application of the method of non-linear mappings for NNLO differential calculations at hadron colliders.• The real (σ R ij→Hk ): Corresponding to the emission of an extra particle k.• The virtual (σ V ij→H ): Corresponding to the emission and re-absorption of a virtual particle.At NNLO there are three separate contributions (see fig. 3):• The double real (σ RR ij→Hkl ): Corresponding to the emission of two particles k and l.• The real-virtual (σ RV ij→Hk ): Corresponding to the emission of one particle k as well as the emission and reabsorption of a virtual particle.• The double virtual (σ V V ij→H ): Corresponding to the emission and re-absorption of two virtual particles.Real and virtual corrections suffer from infra-red as well as ultra-violet divergences. We use conventional dimensional regularization with d = 4 − 2 to regularize such divergences, which then appear as poles in . More specifically ultra-violet divergences present in virtual

Morphological changes during development, tissue repair, and disease largely rely on coordinated cell movements and are controlled by the tissue environment. Epithelial cell sheets are often subjected to large scale deformation during tissue formation. The active mechanical environment in which epithelial cells operate have the ability to promote collective oscillations, but how these cellular movements are generated and relate to collective migration remains unclear. Here, combining in vitro experiments and computational modelling we describe a novel mode of collective oscillations in confined epithelial tissues where the oscillatory motion is the dominant contribution to the cellular movements. We show that epithelial cells exhibit large-scale coherent oscillations when constrained within micro-patterns of varying shapes and sizes, and that their period and amplitude are set by the smallest confinement dimension. Using molecular perturbations, we then demonstrate that force transmission at cell-cell junctions and its coupling to cell polarity are pivotal for the generation of these collective movements. We find that the resulting tissue deformations are sufficient to trigger mechanotransduction within cells, potentially affecting a wide range of cellular processes.The formation of multicellular patterns of moving cells in living tissues is a hallmark of many developmental and pathological processes including morphogenesis, tissue regeneration, and tumourigenesis 1,2,3 . The ability of the cells to coordinate their motion over large scales 2,4 enables the rapid transmission of mechanical information across the tissue, for example during tissue invagination driven by acto-myosin contractions 5 , gastrulation 6 , the propagation of velocity waves far from the free edge of migrating monolayers 7,8 or the transmission of contact-guidance signals away from localised topographical cues 9 . It is * These authors contributed equally to this work