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"Cell Behavior"
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Mobile phone behavior
\"This book provides the first comprehensive introduction to the newly-emerging science of mobile phone behavior. It presents the unexpected complexity of human mobile phone behavior through four basic aspects of mobile phone usage (users, technologies, activities, and effects), and then explores four major domains of such behavior (medicine, business, education, and everyday life). Chapters open with thoughts on mobile phone usage and behavior from interviews with cell phone users, then present a series of scientific studies, synthesized knowledge, and real-life cases, concluding with complex but highly readable analyses of each aspect of mobile phone behavior. Readers should achieve two intellectual goals: gaining a usable knowledge of the complexity of mobile phone behaviour, and developing the skills to analyze the complexity of mobile phone usage - and further technological behaviors\"-- Provided by publisher.
Book
Anti–neurofascin-155 IgG4 antibodies prevent paranodal complex formation in vivo
Neurofascin-155 (Nfasc155) is an essential glial cell adhesion molecule expressed in paranodal septate-like junctions of peripheral and central myelinated axons. The genetic deletion of Nfasc155 results in the loss of septate-like junctions and in conduction slowing. In humans, IgG4 antibodies against Nfasc155 are implicated in the pathogenesis of chronic inflammatory demyelinating polyneuropathy (CIDP). These antibodies are associated with an aggressive onset, a refractoriness to intravenous immunoglobulin, and tremor of possible cerebellar origin. Here, we examined the pathogenic effects of patient-derived anti-Nfasc155 IgG4. These antibodies did not inhibit the ability of Nfasc155 to complex with its axonal partners contactin-1/CASPR1 or induce target internalization. Passive transfer experiments revealed that IgG4 antibodies target Nfasc155 on Schwann cell surface, and diminished Nfasc155 protein levels and prevented paranodal complex formation in neonatal animals. In adult animals, chronic intrathecal infusions of antibodies also induced the loss of Nfasc155 and of paranodal specialization and resulted in conduction alterations in motor nerves. These results indicate that anti-Nfasc155 IgG4 perturb conduction in absence of demyelination, validating the existence of paranodopathy. These results also shed light on the mechanisms regulating protein insertion at paranodes.
Journal Article
Genetic and pharmacological inhibition of microRNA-92a maintains podocyte cell cycle quiescence and limits crescentic glomerulonephritis
Crescentic rapidly progressive glomerulonephritis (RPGN) represents the most aggressive form of acquired glomerular disease. While most therapeutic approaches involve potentially toxic immunosuppressive strategies, the pathophysiology remains incompletely understood. Podocytes are glomerular epithelial cells that are normally growth-arrested because of the expression of cyclin-dependent kinase (CDK) inhibitors. An exception is in RPGN where podocytes undergo a deregulation of their differentiated phenotype and proliferate. Here we demonstrate that microRNA-92a (miR-92a) is enriched in podocytes of patients and mice with RPGN. The CDK inhibitor p57
Kip2
is a major target of
miR-92a
that constitutively safeguards podocyte cell cycle quiescence. Podocyte-specific deletion of
miR-92a
in mice de-repressed the expression of p57
Kip2
and prevented glomerular injury in RPGN. Administration of an anti-miR-92a after disease initiation prevented albuminuria and kidney failure, indicating miR-92a inhibition as a potential therapeutic strategy for RPGN. We demonstrate that miRNA induction in epithelial cells can break glomerular tolerance to immune injury.
Crescentic rapidly progressive glomerulonephritis is a severe form of glomerula disease characterized by podocyte proliferation and migration. Here Henique et al. demonstrate that inhibition of miRNA-92a prevents kidney failure by promoting the expression of CDK inhibitor p57
Kip2
that regulates podocyte cell cycle.
Journal Article
How gluttonous cell aggregates clear substrates coated with microparticles
We study the spreading of cell aggregates deposited on adhesive substrates decorated with microparticles (MPs). A cell monolayer expands around the aggregate. The cells on the periphery of the monolayer take up the MPs, clearing the substrate as they progress and forming an aureole of cells filled with MPs. We study the dynamics of spreading and determine the width of the aureole and the level of MP internalization in cells as a function of MP size, composition, and density. From the radius and width of the aureole, we quantify the volume fraction of MPs within the cell, which leads to an easy, fast, and inexpensive measurement of the cell – particle internalization.
Journal Article
Effect of Arabinogalactan Proteins from the Root Caps of Pea and Brassica napus on Aphanomyces euteiches Zoospore Chemotaxis and Germination
Root tips of many plant species release a number of border, or border-like, cells that are thought to play a major role in the protection of root meristem. However, little is currently known on the structure and function of the cell wall components of such root cells. Here, we investigate the sugar composition of the cell wall of the root cap in two species: pea (Pisum sativum), which makes border cells, and Brassica napus, which makes border-like cells. We find that the cell walls are highly enriched in arabinose and galactose, two major residues of arabinogalactan proteins. We confirm the presence of arabinogalactan protein epitopes on root cap cell walls using immunofluorescence microscopy. We then focused on these proteoglycans by analyzing their carbohydrate moieties, linkages, and electrophoretic characteristics. The data reveal (1) significant structural differences between B. napus and pea root cap arabinogalactan proteins and (2) a cross-link between these proteoglycans and pectic polysaccharides. Finally, we assessed the impact of root cap arabinogalactan proteins on the behavior of zoospores of Aphanomyces euteiches, an oomycetous pathogen of pea roots. We find that although the arabinogalactan proteins of both species induce encystment and prevent germination, the effects of both species are similar. However, the arabinogalactan protein fraction from pea attracts zoospores far more effectively than that from B. napus. This suggests that root arabinogalactan proteins are involved in the control of early infection of roots and highlights a novel role for these proteoglycans in root-microbe interactions.
Journal Article
Editorial: Ralstonia solanacearum–Plant Interactions: Plant Defense Responses, Virulence Mechanisms and Signaling Pathways
Editorial on the Research TopicRalstonia solanacearum–Plant Interactions: Plant Defense Responses, Virulence Mechanismsand Signaling Pathways
Journal Article
Methanol induces cytosolic calcium variations, membrane depolarization and ethylene production in arabidopsis and tobacco
Abstract
Background and Aims
Methanol is a volatile organic compound released from plants through the action of pectin methylesterases (PMEs), which demethylesterify cell wall pectins. Plant PMEs play a role in developmental processes but also in responses to herbivory and infection by fungal or bacterial pathogens. However, molecular mechanisms that explain how methanol could affect plant defences remain poorly understood.
Methods
Using cultured cells and seedlings from Arabidopsis thaliana and tobacco BY2 expressing the apoaequorin gene, allowing quantification of cytosolic Ca2+, a reactive oxygen species (ROS) probe (CLA, Cypridina luciferin analogue) and electrophysiological techniques, we followed early plant cell responses to exogenously supplied methanol applied as a liquid or as volatile.
Key Results
Methanol induces cytosolic Ca2+ variations that involve Ca2+ influx through the plasma membrane and Ca2+ release from internal stores. Our data further suggest that these Ca2+ variations could interact with different ROS and support a signalling pathway leading to well known plant responses to pathogens such as plasma membrane depolarization through anion channel regulation and ethylene synthesis.
Conclusions
Methanol is not only a by-product of PME activities, and our data suggest that [Ca2+]cyt variations could participate in signalling processes induced by methanol upstream of plant defence responses.
Journal Article
Mechanical induction of the tumorigenic b-catenin pathway by tumour growth pressure
The tumour microenvironment may contribute to tumorigenesis owing to mechanical forces such as fibrotic stiffness or mechanical pressure caused by the expansion of hyper-proliferative cells 1,2. Here we explore the contribution of the mechanical pressure exerted by tumour growth onto non-tumorous adjacent epithe-lium. In the early stage of mouse colon tumour development in the Notch 1 Apc 1/1638N mouse model, we observed mechanistic pressure stress in the non-tumorous epithelial cells caused by hyper-proliferative adjacent crypts overexpressing active Notch, which is associated with increased Ret and b-catenin signalling. We thus developed a method that allows the delivery of a defined mechanical pressure in vivo, by subcutaneously inserting a magnet close to the mouse colon. The implanted magnet generated a magnetic force on ultra-magnetic liposomes, stabilized in the mesench-ymal cells of the connective tissue surrounding colonic crypts after intravenous injection. The magnetically induced pressure quantitatively mimicked the endogenous early tumour growth stress in the order of 1,200 Pa, without affecting tissue stiffness, as monitored by ultrasound strain imaging and shear wave elastography. The exertion of pressure mimicking that of tumour growth led to rapid Ret activation and downstream phosphorylation of b-catenin on Tyr654, imparing its interaction with the E-cadherin in adhe-rens junctions, and which was followed by b-catenin nuclear trans-location after 15 days. As a consequence, increased expression of b-catenin-target genes was observed at 1 month, together with crypt enlargement accompanying the formation of early tumorous aberrant crypt foci. Mechanical activation of the tumorigenic b-catenin pathway suggests unexplored modes of tumour propagation based on mechanical signalling pathways in healthy epithelial cells surrounding the tumour, which may contribute to tumour heterogeneity. To test the tumorous impact of early tumour growth pressure on non-tumorous epithelial tissues in vivo, apart from the mechanical stiffness characteristic of the microenvironment of late tumours 1-6
Journal Article
Profiling Dynamic Patterns of Single‐Cell Motility
Cell motility plays an essential role in many biological processes as cells move and interact within their local microenvironments. Current methods for quantifying cell motility typically involve tracking individual cells over time, but the results are often presented as averaged values across cell populations. While informative, these ensemble approaches have limitations in assessing cellular heterogeneity and identifying generalizable patterns of single‐cell behaviors, at baseline and in response to perturbations. In this study, CaMI is introduced, a computational framework designed to leverage the single‐cell nature of motility data. CaMI identifies and classifies distinct spatio‐temporal behaviors of individual cells, enabling robust classification of single‐cell motility patterns in a large dataset (n = 74 253 cells). This framework allows quantification of spatial and temporal heterogeneities, determination of single‐cell motility behaviors across various biological conditions and provides a visualization scheme for direct interpretation of dynamic cell behaviors. Importantly, CaMI reveals insights that conventional cell motility analyses may overlook, showcasing its utility in uncovering robust biological insights. Together, a multivariate framework is presented to classify emergent patterns of single‐cell motility, emphasizing the critical role of cellular heterogeneity in shaping cell behaviors across populations. Authors present CaMI, a novel computational framework designed to leverage single‐cell motility to deduce novel biological insights. CaMI identifies distinct spatio‐temporal behaviors of cells to enable robust classification of cell motility patterns. Furthermore, CaMI provides a means to directly compute cellular heterogeneity, quantify single‐cell behaviors across multiple conditions, and a visualization scheme for direct interpretation of emergent cell behaviors.
Journal Article
Deciphering the Dynamics of Epithelial-Mesenchymal Transition and Cancer Stem Cells in Tumor Progression
Purpose of Review
The epithelial-mesenchymal transition (EMT) and the generation of cancer stem cells (CSCs) are two fundamental aspects contributing to tumor growth, acquisition of resistance to therapy, formation of metastases, and tumor relapse. Recent experimental data identifying the circuits regulating EMT and CSCs has driven the development of computational models capturing the dynamics of these circuits, and consequently various aspects of tumor progression.
Recent Findings
We review the contribution made by these models in (a) recapitulating experimentally observed behavior, (b) making experimentally testable predictions, and (c) driving emerging notions in the field, including the emphasis on the aggressive potential of hybrid epithelial-mesenchymal (E/M) phenotype(s). We discuss dynamical and statistical models at intracellular and population level relating to dynamics of EMT and CSCs, and those focusing on interconnections between these two processes.
Summary
These models highlight the insights gained via mathematical modeling approaches and emphasizes that the connections between hybrid E/M phenotype(s) and stemness can be explained by analyzing underlying regulatory circuits. Such experimentally curated models have the potential of serving as platforms for better therapeutic design strategies.
Journal Article