Bulletin of the American Physical Society
APS March Meeting 2010
Volume 55, Number 2
Monday–Friday, March 15–19, 2010; Portland, Oregon
Session X7: Waves in Actin Dynamics |
Hide Abstracts |
Sponsoring Units: DPB Chair: Martin Falcke, Delbruck Institute for Molecular Medicine Room: Portland Ballroom 254 |
Thursday, March 18, 2010 2:30PM - 3:06PM |
X7.00001: Soft Brains, Signal Amplification through Noise, and Taking the Brain by its Horns Invited Speaker: For the brain's viscoelastic properties single cell measurements reveal the softness of neurons and Glial cells, which consequentially rules out the notion of Glial cells as structural support. In contrary the mechanosensitive neurons follow in their growth and development the even softer Glial cells by inverse durotaxis. The motion of growth cones, the leading motile structures of growing neurons, results from a competition of stochastic processes responsible for forward and backward movement. Noise tuning of the growth cone's stochastic fluctuations increases neuronal sensitivity to chemotaxis. The forces underlying the spatial interplay of random actin polymerization driving the forward motion and molecular motor-based retrograde flow responsible for stochastic retraction are measured either by applying conservation laws (continuity equation and force balance) to the cytoskeletal dynamics of GFP-actin transfected growth cones or by directly detecting these forces with AFM. By a simple mechanical lever arm effect weak optical gradient forces acting on the spike-like filopodia, the exploring ``horns'' of growth cones, are sufficient to control the direction of growth cones' stochastic forward motion. [Preview Abstract] |
Thursday, March 18, 2010 3:06PM - 3:42PM |
X7.00002: Shaping Cells by Force and Rigidity through Protein Stretching Invited Speaker: Control of cell morphology involves the integration of mechanical sensing and different types of cell motility to produce the desired shape of the organism. Nanometer level analyses of cell behavior have revealed only a limited number of types of motility involving complex mechanochemical steps (D\"{o}bereiner, et al., 2004. \textit{Phys Rev Letters} \textbf{93}, 108105). For example, cell spreading on matrix-coated surfaces have revealed three different types of motility, an initial blebbing, continuous spreading, and periodic contraction motility dependent upon myosin II. Matrix forces are sensed by protein stretching through two different cytoplasmic mechanisms. One example is the activation of protein phosphorylation by stretching (Sawada et al., 2006. Cell 127, 1015). Secondly, the stretching of proteins can unveil binding sites such as the stretching of talin causing the increased binding of vinculin (del Rio et al., 2009. Science 323, 638). Stretching controls different motility types and it is important to understand each type of motility at the nanometer level. [Preview Abstract] |
Thursday, March 18, 2010 3:42PM - 4:18PM |
X7.00003: Protrusion phenotypes driven by actin-membrane interaction Invited Speaker: We present a mathematical model for the leading edge motion of migrating cells. A variety of dynamic regimes is observed experimentally, e.g. uniform oscillations and local protrusions or undulations traveling along the plasma membrane. Our model reproduces those states of movement. We calculate the force that single actin filaments of different contour length in the lamellipodium exert on the membrane. The total actin network force is not only length dependent but also determined by the attachment dynamics of the filaments. The membrane motion then results from the balance of this actin network force, viscous drag force and membrane tension in every point along the membrane. A change in model parameters like the polymerization velocity of actin filaments can lead to a change in the dynamic state of membrane motion. Accordingly, in experiments with epithelial cells, different morphodynamic patterns are observed under wild type conditions and in cells expressing constitutively active Rac. [Preview Abstract] |
Thursday, March 18, 2010 4:18PM - 4:54PM |
X7.00004: Guided by curvature: the membrane shape coupled to cytoskeleton Invited Speaker: We present theoretical models whereby the self-organization of cortical actin polymerization is controlled by curvature-sensitive protein complexes. In these systems the membrane is both shaped by the actin forces and curved membrane proteins, and in turn guides the cytoskeletal activity. This feedback is shown to give rise to membrane oscillations and waves in a number of different systems, and is compared to experimental observations of such waves. [Preview Abstract] |
Thursday, March 18, 2010 4:54PM - 5:30PM |
X7.00005: Dendritic Actin Nucleation Causes Traveling Waves and Patches Invited Speaker: Reversible polymerization of the intracellular protein actin into semiflexible filaments is crucial for cell motion and environmental sensing. Recent studies have shown that polymerized actin can spontaneously form traveling waves and/or moving patches. I investigate possible mechanisms for such phenomena by numerically simulating the ``dendritic nucleation'' model of actin network growth. The simulations treat the growth of an actin network on a flat portion of a cell membrane, using a stochastic-growth method which calculates an explicit three-dimensional network structure. The calculations treat processes including filament growth, capping, branching, severing, and Brownian motion. The dynamics of membrane proteins stimulating actin polymerization are also included: they diffuse in the membrane, and detach/deactivate in the presence of polymerized actin. The simulations show three types of polymerized-actin behavior: 1) traveling waves, 2) coherently moving patches, and 3) random fluctuations with occasional moving patches. Wave formation is favored at low free-actin concentrations by a long reattachment time for the membrane proteins, and by weakness of the attractive interaction between filaments and the membrane. Raising the free-actin concentration results in a randomly varying distribution of polymerized actin. Lowering the free-actin concentration below the optimal value for waves causes the waves to break up into patches which, however, move coherently. Effects of similar magnitude are predicted when other intracellular protein concentrations are varied. Diffusion of the membrane proteins slows the waves, and, if fast enough, stops them completely, resulting in the formation of a static spot. [Preview Abstract] |
Follow Us |
Engage
Become an APS Member |
My APS
Renew Membership |
Information for |
About APSThe American Physical Society (APS) is a non-profit membership organization working to advance the knowledge of physics. |
© 2024 American Physical Society
| All rights reserved | Terms of Use
| Contact Us
Headquarters
1 Physics Ellipse, College Park, MD 20740-3844
(301) 209-3200
Editorial Office
100 Motor Pkwy, Suite 110, Hauppauge, NY 11788
(631) 591-4000
Office of Public Affairs
529 14th St NW, Suite 1050, Washington, D.C. 20045-2001
(202) 662-8700