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For more than 30 years, Current Topics in Developmental Biology has provided a forum for dissemination and discussion of new ideas and thought in developmental biology. Bringing together a series of articles on the structural, functional, and developmental characteristics of epithelials, this thematic volume represents a timely and valuable contribution to an exciting and multidisciplinary field of study. Because defects in epithelial function and growth control play a major role in human disease-cancerous tumors, spina bifida, cardiac malformations, for example-this volume will be of particular interest to researchers working in cancer drug design and development and those working in therapeutic areas to treat developmental abnormalities. Coverage of current research findings and thought on cell-cell and cell-extracellular matrix interactions gives researchers a better understanding of the processes of remodeling and morphogenesis, which are critical to the development of drugs aimed at disrupting the early formation and proliferation of cancerous tumors Inclusion of chapters that discuss the most contemporary thought on cell polarity and tissue morphogenesis, providing researchers with a better understanding of the control of cellular organization and polarity (particularly important to researchers who are developing treatments for developmental abnormalities and those working in cancer drug development) Use of a variety of animal models, allowing researchers to compare and contrast the molecular mechanisms that underlie cell-cell and cell-extracelluar matrix interactions in a variety of research models
This manual constitutes the proceedings of the 11th Growth Factor and Signal Transduction Symposium, held in Iowa in 2002, and it presents 22 papers and 10 posters. It focuses on the molecular and cellular mechanisms of tissue remodelling, centring around the themes of angiogenesis, wound healing, and hormone-regulated remodelling.
Bringing together a series of articles on the structural, functional, and developmental characteristics of epithelia, this volume represents a timely and valuable contribution to a growing field of study.
This book describes the shape formation of living organisms using mathematical models. Genes are deeply related to the shape of living organisms, and elucidation of a pathway of shape formation from genes is one of the fundamental problems in biology. Mathematical cell models are indispensable tools to elucidate this problem. The book introduces two mathematical cell models, the cell center model and the vertex model, with their applications. The cell center model is applied to elucidate the formation of neat cell arrangements in epidermis, cell patterns consisting of heterogeneous-sized cells, capillary networks, and the branching patterns of blood vessels. The vertex model is applied to elucidate the wound healing mechanisms of the epithelium and ordered pattern formation involving apoptosis. Pattern formation with differential cell adhesion is also described. The vertex model is then extended from a two-dimensional (2D) to a three-dimensional (3D) model. A cell aggregate involving a large cavity is described to explain the development of the mammalian blastocyst or the formation of an epithelial vesicle. Epithelial tissues and the polarity formation process of the epithelium are also explained. The vertex model also recapitulates active remodeling of tissues and describes the twisting of tissue that contributes to understanding the cardiac loop formation of the embryonic tube. The book showcases that mathematical cell models are indispensable tools to understand the shape formation of living organisms. Successful contribution of the mathematical cell models means that the remodeling of collective cells is self-construction. Examining the successive iterations of self-constructions leads to understanding the remarkable and mysterious morphogenesis that occurs during the development of living organisms. The intended readers of this book are not only theoretical or mathematical biologists, but also experimental and general biologists, including undergraduate and postgraduate students who are interested in the relationship between genes and morphogenesis.
Epithelial tissues exhibit a diverse range of morphologies that support specific functions within the body. During morphogenesis, cells within a tissue must coordinately receive and respond to spatial information; this ability is reflected by the polarization of molecules, structures, or behaviors within the plane of the tissue, a property known as planar cell polarity. This dissertation describes the morphogenesis of denticle-producing cells in the Drosophila embryo, which display a planar polarized organization of the actin-based denticle structure, adherens junctions, and the microtubule cytoskeleton. Denticle-producing cells undergo changes in morphology accompanied by polarized remodeling of cellular junctions. Fat, an evolutionarily conserved cadherin, was required for all of these aspects of planar polarized cell organization and behavior, suggesting that Fat signaling provides a common spatial cue that influences diverse classes of cell biological processes involving the cytoskeleton, adhesion, and contractility. Polarized structures were readily visible using fixed and live imaging of intact embryos, and I present quantitative methods for describing the behavior of these structures over time. My findings additionally implicate the myosin Dachs, Hippo/Warts signaling, and Notch activity as mechanisms that influence planar polarity in the embryo. The work presented in this dissertation demonstrates the tractability of denticle-producing cells as a model system for studying planar cell polarity, and has identified the Fat cadherin as a molecular starting point from which to investigate diverse mechanisms of epithelial morphogenesis.
Cells in the developing embryo depend on signals from the extracellular environment to help guide their differentiation. An important mediator in this process is the extracellular matrix – secreted macromolecules that interact to form large protein networks outside the cell. During development, the extracellular matrix serves to separate adjacent cell groups, participates in establishing morphogenic gradients, and, through its ability to interact directly will cell-surface receptors, provides developmental clocks and positional information. This volume discusses how the extracellular matrix influences fundamental developmental processes and how model systems can be used to elucidate ECM function. The topics addressed range from how ECM influences early development as well as repair processes in the adult that recapitulate developmental pathways.
Branching morphogenesis, the creation of branched structures in the body, is a key feature of animal and plant development. This book brings together, for the first time, expert researchers working on a variety of branching systems to present a state-of-the-art view of the mechanisms that control branching morphogenesis. Systems considered range from single cells, to blood vessel and drainage duct systems to entire body plans, and approaches range from observation through experiment to detailed biophysical modelling. The result is an integrated overview of branching.
Epithelial-mesenchymal transition (EMT) regulates the cellular processes of migration, growth, and proliferation - as well as the collective cellular process of tissue remodeling - in response to mechanical and chemical stimuli in the cellular microenvironment. Cells of the epithelium form cell-cell junctions with adjacent cells to function as a barrier between the body and its environment. By distributing localized stress throughout the tissue, this mechanical coupling between cells maintains tensional homeostasis in epithelial tissue structures and provides positional information for regulating cellular processes. Whereas in vitro and in vivo models fail to capture the complex interconnectedness of EMT-associated signaling networks, previous computational models have succinctly reproduced components of the EMT program. In this work, we have developed a computational framework to evaluate the mechanochemical signaling dynamics of EMT at the molecular, cellular, and tissue scale. First, we established a model of cell-matrix and cell-cell feedback for predicting mechanical force distributions within an epithelial monolayer. These findings suggest that tensional homeostasis is the result of cytoskeletal stress distribution across cell-cell junctions, which organizes otherwise migratory cells into a stable epithelial monolayer. However, differences in phenotype-specific cell characteristics led to discrepancies in the experimental and computational observations. To better understand the role of mechanical cell-cell feedback in regulating EMT-dependent cellular processes, we introduce an EMT gene regulatory network of key epithelial and mesenchymal markers, E-cadherin and N-cadherin, coupled to a mechanically-sensitive intracellular signaling cascade. Together these signaling networks integrate mechanical cell-cell feedback with EMT-associated gene regulation. Using this approach, we demonstrate that the phenotype-specific properties collectively account for discrepancies in the computational and experimental observations. Additionally, mechanical cell-cell feedback suppresses the EMT program, which is reflected in the gene expression of the heterogeneous cell population. Together, these findings advance our understanding of the complex interplay in cell-cell and cell-matrix feedback during EMT of both normal physiological processes as well as disease progression.
Epithelial-mesenchymal transition (EMT) is a conversion that facilitates organ morphogenesis and tissue remodeling in physiological processes such as embryonic development and wound healing. A similar phenotypic conversion is also detected in fibrotic diseases and neoplasia, which is associated with disease progression. EMT in cancer epithelial cells often seems to be an incomplete and bi-directional process. In this Review, we discuss the phenomenon of EMT as it pertains to tumor development, focusing on exceptions to the commonly held rule that EMT promotes invasion and metastasis. We also highlight the role of the RAS-controlled signaling mediators, ERK1, ERK2 and PI3-kinase, as microenvironmental responsive regulators of EMT.