Bulletin of the American Physical Society
APS March Meeting 2015
Volume 60, Number 1
Monday–Friday, March 2–6, 2015; San Antonio, Texas
Session Z46: Invited Session: Mechanical Interactions and Pattern Formation in Multicellular Systems |
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Sponsoring Units: DBIO Chair: Ingmar Riedel-Kruse, Stanford University Room: 217A |
Friday, March 6, 2015 11:15AM - 11:51AM |
Z46.00001: Tissue mechanics and dynamics during development Invited Speaker: Frank Julicher The fly wing is an important model system for the study of tissue dynamics during development. During pupal stages, the early fly wing undergoes a spectacular dynamic reorganization that involves cell flows, cell divisions and cell shape changes. In this dynamic process, the final shape of the wing is generated. We characterize tissue remodelling by the contributions of specific cellular processes such as cell shape changes and cell neighbour exchanges to macroscopic shear at different times. We discuss the dynamics and the mechanics of this dynamic tissue using an active medium theory that captures the essential physics of tissue remodeling. Our work suggests that local tissue contraction together with anisotropic active processes drive tissue remodelling in the fly wing. This process is guided by external stresses mediated via elastic attachments of the tissue to an external scaffold. We test our model by experiments in which perturbations are imposed by laser ablation or by mutant conditions. [Preview Abstract] |
Friday, March 6, 2015 11:51AM - 12:27PM |
Z46.00002: Spatiotemporal control of the forces that drive cell rearrangements within multicellular tissues Invited Speaker: Karen Kasza The local rearrangements of cells within multicellular tissues are actively driven by forces generated in the actin-myosin cytoskeleton. During development, these forces are patterned to bias or orient cell rearrangements, resulting in changes in tissue shape and structure that build functional tissues and organs. We use the fruit fly embryo as a model system, where polarized patterns of myosin activity are required for oriented cell rearrangements that drive rapid tissue elongation along the head-to-tail axis. To uncover mechanisms of how active, myosin-generated forces drive cell rearrangement, we quantify how perturbations to myosin activity influence the number, speed, and orientation of rearrangements. First, to investigate microscopic mechanisms by which myosin drives contraction of cell edges to initiate rearrangement, we generated myosin variants predicted to alter the speed at which myosin translocates actin filaments. These myosin variants display slowed turnover dynamics at cell edges and result in decreased numbers of cell rearrangements, indicating a role for myosin-driven actin sliding during rearrangement. Next, to study how myosin activity levels influence cell rearrangements, we generated myosin variants that mimic the active, phosphorylated state of myosin. These variants accelerate rearrangements but, surprisingly, also alter the spatial pattern of forces in the tissue and result in reduced tissue elongation. These myosin variants increase the rate of cell edge contraction but cause defects in the formation of new contacts between cells. Finally, we discuss how higher-order, collective cell rearrangements called rosettes are influenced by these perturbations to myosin activity. \textit{This work is in collaboration with D. Farrell and J. Zallen at the Sloan Kettering Institute.} [Preview Abstract] |
Friday, March 6, 2015 12:27PM - 1:03PM |
Z46.00003: Cell mechanics and non-genetic developmental defects Invited Speaker: M. Shane Hutson Genetic mutations are not the only, nor necessarily the most prevalent route to misregulation of morphogenesis. In fact, remarkably specific developmental defects can be caused by non-specific environmental stress -- e.g., heat shock, anoxia or chemical exposure. I will discuss one example from \textit{Drosophila} embryos in which the funneling from broad-spectrum insult to specific developmental defects can be traced to cell and tissue mechanics. In particular, I will discuss heat shocks applied to \textit{Drosophila} embryos at the onset of gastrulation. These lead to common developmental defects in head involution and germband retraction -- the latter phenocopying U-shaped mutants. Although these heat shocks induce a wide range of transient effects -- on protein synthesis, cytoskeletal structures, and the cell cycle -- morphogenetic movements resume after heat shock and proceed nearly normally for several hours. Then, four to ten hours after heat shock, dramatic holes open between cells in the amnioserosa, disrupting the integrity of this monolayer epithelium. The presence of holes in the amnioserosa at this stage (germband extension) is highly correlated with later defects in retraction of the germband -- a tissue adjacent to the amnioserosa. This observation begs two questions: (1) how does heat-shock of the entire embryo lead to mechanical disruption of this specific tissue; and (2) how does this mechanical disruption lead to morphogenetic defects in adjacent tissues? Using a combination of quantitative live imaging, laser-microsurgery, FRAP and computational models, we find answers to both questions in the underlying cell- and tissue-level mechanics. [Preview Abstract] |
Friday, March 6, 2015 1:03PM - 1:39PM |
Z46.00004: Surface cell expansion drives radial cell intercalations in zebrafish gastrulation Invited Speaker: Carl-Philipp Heisenberg Radial cell intercalations are commonly associated with tissue spreading in many developmental and disease-related processes. Yet, how radial cell intercalations are controlled and function in tissue spreading remains unknown. Here, we use a combination of experiments and theory to analyze radial cell intercalations during doming, the initial spreading of the blastoderm over the yolk cell at early zebrafish gastrulation. Strikingly, we found that radial cell intercalations do not drive doming, but rather determine the viscous relaxation behavior of the blastoderm in response to tissue surface tension (TST)-driven deformation. We further show that radial cell intercalations and, consequently, doming are triggered by surface epithelial cells expanding their surface area and thus reducing TST. Thus, radial cell intercalations are required for translating changes in tissue-scale forces into tissue deformation. [Preview Abstract] |
Friday, March 6, 2015 1:39PM - 2:15PM |
Z46.00005: Glass transition originating from a rigidity transition in confluent biological tissues Invited Speaker: Dapeng Bi Cells must move through tissues in many important biological processes, including embryonic development, cancer metastasis, and wound healing. Often these tissues are dense and a cell's motion is strongly constrained by its neighbors, leading to glassy dynamics. Although there is a density-driven glass transition in self-propelled particle (SPP) models for active matter, these cannot explain liquid-to-solid transitions in confluent tissues, where there are no gaps between cells and the packing fraction remains fixed and equal to unity. We have recently described a different type of rigidity transition that occurs in confluent tissue monolayers in the limit of vanishing cell motility, where the onset of rigidity is governed by changes to single-cell properties such as cell-cell adhesion and cortical tension. Here we alter the model to include cell motility using an equation for polarization similar to those in SPP models. We identify a glass transition line that originates at the critical point of in the rigidity transition, and compare the results to an analytic trap model. The model provides a novel signature for mechanical behavior in confluent tissues, which has been successfully tested in experimental systems. I will also demonstrate that this model provides a framework for studying the Epithelial-to-Mesenchymal transition in cancer invasion and cell sorting during embryonic development. [Preview Abstract] |
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