Bulletin of the American Physical Society
APS March Meeting 2019
Volume 64, Number 2
Monday–Friday, March 4–8, 2019; Boston, Massachusetts
Session K64: Active and Living Matter IFocus
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Sponsoring Units: DBIO Chair: Jeremie Palacci, University of California, San Diego Room: BCEC 259B |
Wednesday, March 6, 2019 8:00AM - 8:36AM |
K64.00001: Award for Outstanding Doctoral Thesis Research in Biological Physics Talk: Mechanics and energetics of the bacterial flagellar motor Invited Speaker: Jasmine Nirody The bacterial flagellar motor (BFM) is an ion-powered nanomachine that drives swimming in many bacteria. This protein complex is comprised of several transmembrane rings connected to a long flagellar filament by a flexible hook. Rotation is known to occur via an interaction between one or more membrane-embedded “stator” units, and protein spokes on the periphery of the spinning “rotor” ring. In this talk, I will touch on three features of the motor: (1) its fundamental mechanochemical cycle, (2) the dynamic remodelling of motor structure in response to its environment, and (3) the efficiency of the motor. First, taking into account all the structural and dynamic biophysical experimental evidence to date, we present a mechanically-specific, testable model of the motor’s mechanism of torque generation. We validate this theoretical model of the BFM’s mechanochemical cycle against experiments done on motors with a single stator. Second, we extend this base model to consider the behavior of multi-stator motors. Stator units have been shown to dynamically bind and leave the motor. We present several recent experiments that shine light on the nature of this complex process, which is influenced by several factors, including the ion gradient, external load, and motor speed. Finally, we also discuss experiments directly measuring the relationship between ion flux through the membrane and motor speed, towards answering the question of whether the motor is loosely or tightly coupled to ion flux — that is, whether each ion passage constitutes a fully efficient power stroke. |
Wednesday, March 6, 2019 8:36AM - 9:12AM |
K64.00002: Invariance properties of bacterial random walks inside domains with variable geometry and structural disorder Invited Speaker: Roberto Di Leonardo Motile cells often explore natural environments characterized by a high degree of structural complexity. Moreover cell motility is also intrinsically noisy due to spontaneous random reorientation and speed fluctuations. The interplay of different noise sources gives rise to complex dynamical behavior that can be strongly sensitive to details and hard to model quantitatively. In striking contrast to this general picture we show that the mean residence time of swimming bacteria inside artificial complex microstructures |
Wednesday, March 6, 2019 9:12AM - 9:24AM |
K64.00003: Spontaneously oscillating synthetic cilia Isabella Guido, Andrej Vilfan, Ramin Golestanian, Eberhard Bodenschatz, Kazuhiro Oiwa Cilia and flagella produce rapid and regular bending waves responsible for the propulsion of organisms in fluids or for the promotion of fluid transport. It is known that the main contribution to their beating is due to motor proteins, dynein, which drives sliding of the microtubule doublets. However, the fundamental mechanism of the dynein-microtubule interaction is still a puzzle. |
Wednesday, March 6, 2019 9:24AM - 9:36AM |
K64.00004: Quantitative in vivo measurements of cerebrospinal fluid flow through perivascular spaces in the brain Jeffrey Tithof, Humberto Mestre, Ting Du, Wei Song, Weiguo Peng, Amanda M Sweeney, Genaro Olveda, John H Thomas, Maiken Nedergaard, Douglas H Kelley Recent discoveries have uncovered a novel route for the flow of cerebrospinal fluid (CSF) through the brain which is important for the removal of protein waste, such as amyloid-β. Characterizing this flow and the mechanisms which reduce it may offer new insight into the development of neurodegenerative diseases, such as Alzheimer’s disease, which are correlated with accumulation of protein waste. CSF enters the brain along perivascular spaces (PVSs) — annular tunnels around arteries — and arterial pulsations are hypothesized to drive these flows, but this has never been quantitatively shown. We perform experiments to measure PVS flows by injecting microspheres into the CSF of living mice, imaging PVSs using two-photon microscopy, and performing particle tracking velocimetry. We also perform line scans to measure arterial pulsations. These measurements offer the first quantitative evidence demonstrating that CSF is driven through PVSs by arterial pulsations. Furthermore, by increasing blood pressure, we observe changes in the arterial pulsations and a net reduction in the CSF flow speed. Our results offer one potential causal mechanism which may contribute to reduced protein waste clearance and development of neurodegenerative diseases. |
Wednesday, March 6, 2019 9:36AM - 9:48AM |
K64.00005: WITHDRAWN ABSTRACT
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Wednesday, March 6, 2019 9:48AM - 10:00AM |
K64.00006: Live cell and in vitro mitotic spindles as arrested liquid crystal tactoids. Sumon Sahu, Bianca Edozie, Patricia Wadsworth, Jennifer Ross Microtubule self-organization is a fundamentally important phenomenon from both physics and biological point of view. One interesting and important structure is the mitotic spindle, a football-shaped structure used to align and ultimately separate the chromosomes during cell division. Recent studies have claimed that the meiotic spindle is internally organized like a liquid crystal tactoid with many, short microtubules that are fluid-like and can coalesce like droplets. Using live cell experiments, we find that the regions of mitotic spindle near the chromosomes are more fluidized, but other regions are arrested. Using photoactivation, we can measure the dynamics of different regions of the spindle and the relative concentration of microtubule-associated proteins and motors as a function of the microtubule concentration. In addition, we use in vitro reconstitution experiments of microtubule polymerization in the presence of a microtubule crosslinker, MAP65, and depletion agents that can form spindle-like structures. Using FRAP experiments, we found that these spindle-like assemblies are not fluid, but rather arrested, unlike liquid crystals. Using this combination of live cell and in vitro reconstitution, we are uncovering the physical organizations of the mitotic spindle. |
Wednesday, March 6, 2019 10:00AM - 10:12AM |
K64.00007: Actin assembly alone can drive inward and outward membrane deformations Camille Simon, Remy Kusters, Valentina Caorsi, Joanny Jean-Francois, Clément Campillo, Julie Plastino, Pierre Sens, Cécile Sykes The cell membrane is able to deform inward, as during the initiation of endocytosis, or outward, as during the formation of filopodia. Interestingly, both deformations are generated by the same branched, Arp2/3-based, polymerizing actin network. How an inward or an outward deformation can be obtained in the same network structure? What are the physical parameters that will trigger the direction of membrane deformation? To address these questions, we use a reconstituted membrane system of liposomes and purified actin. We investigate the conditions under which the actin cytoskeleton induces inward or outward membrane deformations. We reveal that actin dynamics are the essential player of membrane deformations by photo-damaging the actin structure that relaxes membrane shape. Lowering membrane tension is key to produce filopodia-like structures. Oppositely, endocytic-like structures are robust features that only weakly depend on membrane tension. A pulse-chase two color actin experiment and the labeling of the proteins associated to actin reveal the details of network growth during inward or outward membrane deformation. Our results, supported by theoretical models, explain how such deformations depend on a mechanical balance between the membrane and the actin network. |
Wednesday, March 6, 2019 10:12AM - 10:24AM |
K64.00008: Local, biased polymerization kinetics lead to slow axonal transport of actin Nilaj Chakrabarty, Pankaj Dubey, Yong Tang, Archan Ganguly, Kelsey Ladt, Christophe Leterrier, Subhojit Roy, Peter Jung Actin, a key protein constituent of the neuronal cytoskeleton is conveyed along the axon at rates corresponding to slow axonal transport. However, the mechanism of this movement is unknown. Recent advances in live imaging of F-actin and super-resolution imaging has revealed that axonal actin is highly dynamic, undergoing focal assembly, disassembly and elongation bidirectionally along the axon. Actin filaments have an anterograde bias, are locally polymerized and grow with their barbed ends attached to stationary axonal endosomes. We generated the dynamics of axonal actin trail assembly using a model of stochastic filament nucleation and elongation which incorporates imaging data. We then devised a photoactivation simulation to track fluorescently labeled actin in the axon, which closely matches the pulse-chase experiment paradigm. Our simulations predict that local, biased polymerization of actin trails lead to global, anterograde actin transport at rates matching in-vivo pulse-chase experimental rates. Collectively, the simulations and experiments point to local assembly and biased polymerization forming the mechanistic basis of bulk transport. This mechanism is distinct from motor-driven polymer sliding and occurs without any significant contribution from microtubules. |
Wednesday, March 6, 2019 10:24AM - 10:36AM |
K64.00009: Impact of filament dynamics on actomyosin flows Danielle Scheff, Margaret Gardel While myosin driven activity in actin networks has proven to be a good model system for studying active matter, actin filaments have internal dynamics that are less well understood. In cells, filaments continuously depolymerize on one end while repolymerizing on the other, an active process that can both relax stresses by depolymerizing stretched filaments and create forces by driving actin into the cell membrane. Here, we study how this activity affects the ability of actin networks to store energy and propagate forces. Using a minimal system we previously developed, we are able to add actin dynamics to systems composed of both short filaments, which form a liquid crystal, and long ones, which form a contractile-network when in the presence of myosin motors. Preliminary results suggest that filament dynamics cause actomyosin networks to contract uniaxially, implying that dynamic filaments contract through sliding, in contrast to stable filaments which contract through buckling. Simultaneously, dynamics redistribute actin allowing the network to maintain long-lasting contractile flows. |
Wednesday, March 6, 2019 10:36AM - 10:48AM |
K64.00010: Noise induced escape in delay coupled mixed-reality systems Klementyna Szwaykowska, Ira Schwartz, Jason Hindes Networks of coupled subsystems are common in many fields, from biology to epidemiology and robotics. The emergent behaviors of these systems depend on the nature of the interaction and the communication network. It is now well-known that delay in communication between individual agents significantly impacts dynamic pattern formation. In addition, noise propagation through coupling can lead to complex system-wide behaviors. We consider a mixed-reality (MR) system in which delay-coupled real and simulated agents fly together in formation, and show how noise acting on the real agents can induce a large transition in the simulated agents. In order to address this problem, we first analyze a generic model of two weakly delay-coupled dynamical systems. We show how noise in one system can drive a catastrophic state transition in the other, even as the noisy system exhibits only small random oscillations; further, we show how the expected transition time scales as a function of the coupling strength and communication delay. We use an analogous approach to study changes in the flight formation of MR agents. |
Wednesday, March 6, 2019 10:48AM - 11:00AM |
K64.00011: Modeling nonequilibrium self-assembly in the cell through reaction-diffusion simulation Matthew Varga, Osman Yogurtcu, Margaret Johnson In diverse cellular pathways including clathrin-mediated endocytosis (CME) and viral bud formation, cytosolic proteins must self-assemble and induce membrane deformation. These essential processes require localization to the membrane at particular times within the cell, relying in part on the nonequilibrium activity of energy consuming kinases, phosphatases, and ATPases to produce robust and reversible assemblies. Current computational tools for studying self-assembly dynamics are not feasible for simulating cellular dynamics due to the slow time-scales and the dependence on energy-consuming events. We recently developed novel reaction-diffusion algorithms and software that enable detailed computer simulations of nonequilibrium self-assembly over long time-scales. Our simulations of clathrin-coat assembly in CME reveal how the formation of structured lattices impacts the kinetics of assembly, and how localization to the membrane can stabilize large, dynamic assemblies not observed in solution. We also recently developed a relatively simple theory to quantify how localization of protein binding partners to the membrane can dramatically enhance binding, via reduction of dimensionality. Membrane localization can thus provide a trigger for assembly. |
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