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Skinny Videos of Metal-Organic Composition User interfaces Obtained through Lazer Evaporation.
In this review, we address the function of immunoglobulin superfamily cell adhesion molecules (IgCAMs) in epithelia. Work in the Drosophila model system in particular has revealed novel roles for calcium-independent adhesion molecules in the morphogenesis of epithelial tissues. We review the molecular composition of lateral junctions with a focus on their IgCAM components and reconsider the functional roles of epithelial lateral junctions. The epithelial IgCAMs discussed in this review have well-defined roles in the nervous system, particularly in the process of axon guidance, suggesting functional overlap and conservation in mechanism between that process and epithelial remodelling. We expand on the hypothesis that epithelial occluding junctions and synaptic junctions are compositionally equivalent and present a novel hypothesis that the mechanism of epithelial cell (re)integration and synaptic junction formation are shared. We highlight the importance of considering non-cadherin-based adhesion in our understanding of the mechanics of epithelial tissues and raise questions to direct future work. This article is part of the discussion meeting issue 'Contemporary morphogenesis'.Tissue folding is a fundamental process that sculpts a simple flat epithelium into a complex three-dimensional organ structure. Whether it is the folding of the brain, or the looping of the gut, it has become clear that to generate an invagination or a fold of any form, mechanical asymmetries must exist in the epithelium. These mechanical asymmetries can be generated locally, involving just the invaginating cells and their immediate neighbours, or on a more global tissue-wide scale. Here, we review the different mechanical mechanisms that epithelia have adopted to generate folds, and how the use of precisely defined mathematical models has helped decipher which mechanisms are the key driving forces in different epithelia. This article is part of a discussion meeting issue 'Contemporary morphogenesis'.The mammalian preimplantation embryo is a highly tractable, self-organizing developmental system in which three cell types are consistently specified without the need for maternal factors or external signals. Studies in the mouse over the past decades have greatly improved our understanding of the cues that trigger symmetry breaking in the embryo, the transcription factors that control lineage specification and commitment, and the mechanical forces that drive morphogenesis and inform cell fate decisions. These studies have also uncovered how these multiple inputs are integrated to allocate the right number of cells to each lineage despite inherent biological noise, and as a response to perturbations. In this review, we summarize our current understanding of how these processes are coordinated to ensure a robust and precise developmental outcome during early mouse development. This article is part of a discussion meeting issue 'Contemporary morphogenesis'.During tissue morphogenesis, mechanical forces are propagated across tissues, resulting in tissue shape changes. These forces in turn can influence cell behaviour, leading to a feedback process that can be described as self-organizing. Here, I discuss cytoskeletal self-organization and point to evidence that suggests its role in directing force during morphogenesis. During Drosophila mesoderm invagination, the shape of the region of cells that initiates constriction creates a mechanical pattern that in turn aligns the cytoskeleton with the axis of greatest resistance to contraction. Chk inhibitor The wild-type direction of the force controls the shape and orientation of the invaginating mesoderm. Given the ability of the actomyosin cytoskeleton to self-organize, these types of feedback mechanisms are likely to play important roles in a range of different morphogenetic events. This article is part of the discussion meeting issue 'Contemporary morphogenesis'.Cell intercalation is a key topological transformation driving tissue morphogenesis, homeostasis and diseases such as cancer cell invasion. In recent years, much work has been undertaken to better elucidate the fundamental mechanisms controlling intercalation. Cells often use protrusions to propel themselves in between cell neighbours, resulting in topology changes. Nevertheless, in simple epithelial tissues, formed by a single layer of densely packed prism-shaped cells, topology change takes place in an astonishing fashion cells exchange neighbours medio-laterally by conserving their apical-basal architecture and by maintaining an intact epithelial layer. Medio-lateral cell intercalation in simple epithelia is thus an exemplary case of both robustness and plasticity. Interestingly, in simple epithelia, cells use a combinatory set of mechanisms to ensure a topological transformation at the apical and basal sides. This article is part of the discussion meeting issue 'Contemporary morphogenesis'.Cell shape changes are key to observable changes at the tissue level during morphogenesis and organ formation. The major driver of cell shape changes in turn is the actin cytoskeleton, both in the form of protrusive linear or branched dynamic networks and in the form of contractile actomyosin. Over the last 20 years, actomyosin has emerged as the major cytoskeletal system that deforms cells in epithelial sheets during morphogenesis. By contrast, the second major cytoskeletal system, microtubules, have so far mostly been assumed to serve 'house-keeping' functions, such as directed transport or cell division, during morphogenetic events. Here, I will reflect on a subset of studies over the last 10 years that have clearly shown a major direct role for the microtubule cytoskeleton in epithelial morphogenesis, suggesting that our focus will need to be widened to give more attention and credit to this cytoskeletal system in playing an active morphogenetic role. This article is part of a discussion meeting issue 'Contemporary morphogenesis'.Cell polarity is the asymmetric distribution of cellular components along a defined axis. Polarity relies on complex signalling networks between conserved patterning proteins, including the PAR (partitioning defective) proteins, which become segregated in response to upstream symmetry breaking cues. Although the mechanisms that drive the asymmetric localization of these proteins are dependent upon cell type and context, in many cases the regulation of actomyosin cytoskeleton dynamics is central to the transport, recruitment and/or stabilization of these polarity effectors into defined subcellular domains. The transport or advection of PAR proteins by an actomyosin flow was first observed in the Caenorhabditis elegans zygote more than a decade ago. Since then a multifaceted approach, using molecular methods, high-throughput screens, and biophysical and computational models, has revealed further aspects of this flow and how polarity regulators respond to and modulate it. Here, we review recent findings on the interplay between actomyosin flow and the PAR patterning networks in the polarization of the C.
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