Bulletin of the American Physical Society
APS March Meeting 2015
Volume 60, Number 1
Monday–Friday, March 2–6, 2015; San Antonio, Texas
Session W46: Invited Session: Collective Behavior and Jamming in Multi-Cellular Systems |
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Sponsoring Units: DBIO GSNP Chair: Jerry Lee, National Cancer Institute Room: 217A |
Thursday, March 5, 2015 2:30PM - 3:06PM |
W46.00001: Unjamming phase transition in the asthmatic airway epithelium Invited Speaker: Jeffrey Fredberg In asthma, an aberrant injury-repair response of the airway epithelium is pivotal in disease initiation and progression. Although the mechanism remains unclear, classical understanding emphasizes inflammatory events together with delayed epithelial cell differentiation and maturation. Here we reveal a physical mechanism that is not anticipated by that classical picture but dominates dynamics of cells cultured from airway epithelia nonetheless. In the course of maturation of the pseudostratified epithelial layer comprising primary human bronchial epithelial cells from non-asthmatic donors, we show a striking collective cellular behavior in which an immature, hypermobile, unjammed, fluid-like phase undergoes a transition into a mature, quiescent, jammed, solid-like phase. But compressive stresses on the epithelial layer that mimic bronchospasm drive the solid-like phase back to the fluid-like phase. We show, further, that the uncompressed epithelial layer from asthmatic donors exhibit spontaneous collective migration behavior that is similarly striking to that observed in compressed normal cells. However, in this case the migration results from a delay in the innate tendency of the epithelial layer to transition from an unjammed phase into a jammed phase. Moreover, the unjammed state of asthmatic cells accompanies intensified adhesive forces transmitted across cell-cell junctions. We introduce a theory of critical scaling that predicts a priori the existence of the observed phase transition. Surprisingly, this theory predicts the transition to be governed by cell shape and cell-cell adhesive forces in a manner that is paradoxical, but is borne out by our direct experimental observations. Together, these findings establish an unanticipated but rigorous physical foundation for further classification and investigation of epithelial layer behavior in asthma, and likely in other processes in disease or development in which epithelial dynamics play a prominent role. [Preview Abstract] |
Thursday, March 5, 2015 3:06PM - 3:42PM |
W46.00002: Minimization of Thermodynamic Costs in Cancer Cell Invasion Invited Speaker: Robert Austin |
Thursday, March 5, 2015 3:42PM - 4:18PM |
W46.00003: A Nanoengineered Framework for Probing Collective Cell Migration Invited Speaker: Pak Kin Wong The fascinating capability of cellular self-organization (often referred as pattern formation) during tissue morphogenesis and regeneration is a central question in developmental biology, regenerative medicine, and complex systems. How do the cells of a tissue know how to organize into functional tissue structures that are much bigger than themselves? How do the individual cells know what they are supposed to do without a central coordinator or a blueprint?~ Furthermore, relatively little is known about how multicellular systems interpret the mechanical cues in the microenvironment, such as global geometric guidance, local cell-cell interactions, and extracellular matrix properties, to collectively drive the morphogenic process that creates complex tissue structures across multiple length scales. In this talk, I will discuss a nanoengineered framework for investigating the mechanoregulation of tissue morphogenesis, such as the capillary morphogenesis and collective cell migration during wound healing. [Preview Abstract] |
Thursday, March 5, 2015 4:18PM - 4:54PM |
W46.00004: ECM Organization and Cell-Cell Cooperation Invited Speaker: Peter Friedl Single-cell or collective invasion results from coordination of cell shape, deformability and actin dynamics relative to the tissue environment. In monomorphic 3D invasion models in vitro, an obligate step of collective invasion is the degradation of extracellular matrix (ECM). Thereby, the density of the ECM determines the invasion mode of mesenchymal tumor cells. Whereas fibrillar, high porosity ECM enables single-cell dissemination, dense matrix induces cell-cell interaction, leader-follower cell behavior and collective migration as an obligate protease-dependent process. Conversely, in vivo monitored by intravital multiphoton second and third harmonic generation microscopy, tissue microniches provide invasion-promoting tracks that enable collective migration along tracks of least resistance. As main routes, non-destructive contact-guidance is mediated by preformed multi-interface perimuscular, vascular and --neural tracks of 1D, 2D and 3D topography. Consistently, spheroids of mesenchymal melanoma or sarcoma tumor cells switched from single-cell to collective invasion modes when confronted with 3D collagen matrices of increasing density, including gain of cell-to-cell junctions, supracellular polarization, suggesting cell jamming imposed by tissue confinement. Targeting of beta1/beta3 integrins induces unexpected plasticity of invasion, including collective and amoeboid single-cell dissemination, followed by enhanced micrometastasis, implicating a role of integrins in cell-cell cooperation and integrin-independent dissemination as effective route to metastasis. In conclusion, cancer invasion is maintained by physicochemical programs that balance cell-intrinsic adhesion and mechanocoupling with encountered physical space and molecular cues. [Preview Abstract] |
Thursday, March 5, 2015 4:54PM - 5:30PM |
W46.00005: Swarming in the bacterium Pseudomonas aeruginosa Invited Speaker: Joao Xavier The fields of systems and synthetic biology have made great progress towards understanding and engineering biological systems while having the living cell as their central focus. However, many biological functions are multicellular and depend on interactions, both physical and chemical, between cells. We investigate organizing principles of multicellular systems using a prokaryotic model: swarming in Pseudomonas aeruginosa. Swarming is a collective form of surface motility that enables P. aeruginosa colonies to migrate over surfaces. We investigate the molecular mechanisms that confer robustness to swarming using a multidisciplinary approach that combines mathematical modeling, quantitative experiments, microbial genetics and comparative genomics to identify and characterize organizing principles of bacterial multicellularity. These ``design principles'' may inspire the development of robust synthetic multicellular systems that utilize emergent collective behaviors of cell populations to perform functions that individual cells cannot. [Preview Abstract] |
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