Bulletin of the American Physical Society
APS March Meeting 2017
Volume 62, Number 4
Monday–Friday, March 13–17, 2017; New Orleans, Louisiana
Session V49: Multiscale Physics of Cellular RemodelingInvited
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Sponsoring Units: DBIO GSOFT Chair: Lisa Manning, Syracuse University Room: 396 |
Thursday, March 16, 2017 2:30PM - 3:06PM |
V49.00001: Cell intercalation in morphogenesis Invited Speaker: Dinah Loerke TBD [Preview Abstract] |
Thursday, March 16, 2017 3:06PM - 3:42PM |
V49.00002: Frontiers in Fluctuation Spectroscopy: Measuring protein dynamics and protein spatio-temporal connectivity Invited Speaker: Michelle Digman Fluorescence fluctuation spectroscopy has evolved from single point detection of molecular diffusion to a family of microscopy imaging correlation tools (i.e. ICS, RICS, STICS, and kICS) useful in deriving spatial-temporal dynamics of proteins in living cells The advantage of the imaging techniques is the simultaneous measurement of all points in an image with a frame rate that is increasingly becoming faster with better sensitivity cameras and new microscopy modalities such as the sheet illumination technique. A new frontier in this area is now emerging towards a high level of mapping diffusion rates and protein dynamics in the 2 and 3 dimensions. In this talk, I will discuss the evolution of fluctuation analysis from the single point source to mapping diffusion in whole cells and the technology behind this technique. In particular, new methods of analysis exploit correlation of molecular fluctuations originating from measurement of fluctuation correlations at distant points (pair correlation analysis) and methods that exploit spatial averaging of fluctuations in small regions (iMSD). For example the pair correlation fluctuation (pCF) analyses done between adjacent pixels in all possible radial directions provide a window into anisotropic molecular diffusion. Similar to the connectivity atlas of neuronal connections from the MRI diffusion tensor imaging these new tools will be used to map the connectome of protein diffusion in living cells. For biological reaction-diffusion systems, live single cell spatial-temporal analysis of protein dynamics provides a mean to observe stochastic biochemical signaling in the context of the intracellular environment which may lead to better understanding of cancer cell invasion, stem cell differentiation and other fundamental biological processes. [Preview Abstract] |
Thursday, March 16, 2017 3:42PM - 4:18PM |
V49.00003: Force generation within tissues during development Invited Speaker: Karen Kasza During embryonic development, multicellular tissues physically change shape, move, and grow. Changes in epithelial tissue organization are often accomplished by local movements of cells that are driven largely by forces generated by the motor protein myosin II. These forces are patterned to orient cell movements, resulting in changes in tissue shape and organization to build functional tissues and organs. To investigate the mechanisms of force generation \textit{in vivo}, we use the fruit fly embryo as a model system. Spatial patterns of forces orient cell movements to drive rapid tissue elongation along the head-to-tail axis of the embryo. I will describe how studying embryos generated with engineered myosin variants provides insight into where, when, and how forces are generated to efficiently reorganize tissues. We found that a myosin variant that is locked-in to the active or ``on'' state accelerates cell movements, while two mutant myosin variants associated with human disease produce slowed cell movement. These myosin variants all disrupt tissue elongation, but live imaging and biophysical measurements reveal distinct effects on myosin organization and dynamics within cells and uncover mechanisms that control the spatial and temporal patterns of force generation. These studies shed light not only on how defects in force generation contribute to disease but also on physical principles at work in active, living materials. [Preview Abstract] |
Thursday, March 16, 2017 4:18PM - 4:54PM |
V49.00004: Vascular retraction driven by matrix softening Invited Speaker: Megan Valentine We recently discovered we can directly apply physical forces and monitor the downstream responses in a living organism in real time through manipulation of the blood vessels of a marine organism called, \textit{Botryllus schlosseri}. The extracellular matrix (ECM) plays a key role in regulating vascular growth and homeostasis in \textit{Botryllus, }a \quad basal chordate which has a large, transparent extracorporeal vascular network that can encompass areas \textgreater 100 cm$^{\mathrm{2}}$. We have determined that lysyl oxidase 1 (LOX1), which is responsible for cross-linking collagen, is expressed in all vascular cells and is critically important for vascular maintenance. Inhibition of LOX1 activity \textit{in vivo} by the addition of a specific inhibitor, {\ss}-aminopropionitrile (BAPN), caused a rapid, global regression of the entire vascular bed, with some vessels regressing \textgreater 10 mm within 16 hrs. In this talk, I will discuss the molecular and cellular origins of this systemic remodeling event, which hinges upon the ability of the vascular cells to sense and respond to mechanical signals, while introducing this exciting new model system for studies of biological physics and mechanobiology. [Preview Abstract] |
Thursday, March 16, 2017 4:54PM - 5:30PM |
V49.00005: Spreading and contraction in phagocytosis: The role of actin organization and curvature Invited Speaker: Jennifer E. Curtis Phagocytosis is the process used by immune cells to engulf and remove foreign objects from the body. The engulfment is realized by the formation of an actin-driven `phagocytic cup' of the cell membrane, which quickly crawls up and then surrounds the object via constriction. In this study, we resolve the paradox of how actin-driven protrusion of the plasma membrane can co-exist with a contractile actin belt proposed to mechanically-drive the closure of the phagocytic cup. To do this we quantitatively assessed macrophage phagocytic behavior in a planar geometry, a process known as frustrated phagocytosis. Our results reveal that phagocytosis occurs in a binary manner, such that once it is initiated, frustrated phagocytosis proceeds at a prescribed rate, resulting in peak contact areas that correspond to a roughly 225\% increase in apparent cell surface area. Upon reaching their maximum area, the majority of macrophages enter a period of late-stage contraction. During the contraction phase, cells exert significant stress on the underlying substrate. Contraction also corresponds with dramatic reorganization of the F-actin cytoskeleton, in particular the formation of a bundled contractile belt around the cell perimeter. In contrast to other studies of phagocytosis, our work definitively illustrates that whatever signals trigger late-stage phagocytic contraction must be independent of particle size and curvature. Mounting evidence suggests that membrane tension is involved in late-stage signaling. The idea that tension is linked to late-stage contraction is reinforced by our finding that the peak-contact area roughly corresponds to the area threshold that results in increased cortical tension, as measured by Lam et al., and that reducing tension through hypertonic buffer shock enables the cells to spread further before the onset of contraction. [Preview Abstract] |
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