Contractile actomyosin networks are responsible for the production of intracellular forces. There is increasing evidence that bundles of actin filaments form interconnected and interconvertible structures with the rest of the network. In this study, we explored the mechanical impact of these interconnections on the production and distribution of traction forces throughout the cell. By using a combination of hydrogel micropatterning, traction-force microscopy and laser photoablation, we measured the relaxation of traction forces in response to local photoablations. Our experimental results and modeling of the mechanical response of the network revealed that bundles were fully embedded along their entire length in a continuous and contractile network of cortical filaments. Moreover, the propagation of the contraction of these bundles throughout the entire cell was dependent on this embedding. In addition, these bundles appeared to originate from the alignement and coalescence of thin and unattached cortical actin filaments from the surrounding mesh.

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Cells employing amoeboid motility exhibit repetitive cycles of rapid expansion and contraction and apply coordinated traction forces to their environment. Although aspects of this process are well studied, it is unclear how the cell controls the coordination of cell length changes with adhesion to the surface. Here, we develop a simple model to mechanistically explain the emergence of periodic changes in length and spatiotemporal dynamics of traction forces measured in chemotaxing unicellular amoeba, Dictyostelium discoideum. In contrast to the biochemical mechanisms that have been implicated in the coordination of some cellular processes, we show that many features of amoeboid locomotion emerge from a simple mechanochemical model. The mechanism for interaction with the environment in Dictyostelium is unknown and thus, we explore different cell-environment interaction models to reveal that mechanosensitive adhesions are necessary to reproduce the spatiotemporal adhesion patterns. In this modeling framework, we find that the other motility modes, such as smooth gliding, arise naturally with variations in the physical properties of the surface. Thus, our work highlights the prominent role of biomechanics in determining the emergent features of amoeboid locomotion.

Abstract. In-beam and decay-spectroscopy studies of neutron-deficient nuclei near the Z=82 shell closure were carried out using the Fragment Mass Analyzer (FMA) and the Gammasphere array, in conjunction with symmetric fusion reactions and the Recoil Decay Tagging (RDT) technique. The primary motivation was to study properties of 179 Tl and 180 Tl, and their daughter, and grand-daughter isotopes. For the first time, in-beam structures associated with 179 Tl and 180 Tl were observed, as well as γ rays associated with the 180 Tl α decay. No long-lived isomer was identified in 180 Tl, in contrast with the known systematics for the heavier odd-odd Tl isotopes.

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The immersed boundary method is a widely used mixed Eulerian/Lagrangian framework for simulating the motion of elastic structures immersed in viscous fluids. In this work, we consider a poroelastic immersed boundary method in which a fluid permeates a porous, elastic structure of negligible volume fraction, and extend this method to include stress relaxation of the material. The porous viscoelastic method presented here is validated for a prescribed oscillatory shear and for an expansion driven by the motion at the boundary of a circular material by comparing numerical solutions to an analytical solution of the Maxwell model for viscoelasticity. Finally, an application of the modelling framework to cell biology is provided: passage of a cell through a microfluidic channel. We demonstrate that the rheology of the cell cytoplasm is important for capturing the transit time through a narrow channel in the presence of a pressure drop in the extracellular fluid.A porous viscoelastic model for the cell cytoskeleton 2

Contractile actomyosin networks generate intracellular forces essential for the regulation of cell shape, migration, and cell-fate decisions, ultimately leading to the remodeling and patterning of tissues. Although actin filaments aligned in bundles represent the main source of traction-force production in adherent cells, there is increasing evidence that these bundles form interconnected and interconvertible structures with the rest of the intracellular actin network. In this study, we explored how these bundles are connected to the surrounding cortical network and the mechanical impact of these interconnected structures on the production and distribution of traction forces on the extracellular matrix and throughout the cell. By using a combination of hydrogel micropatterning, traction-force microscopy and laser photoablation, we measured the relaxation of the cellular traction field in response to local photoablations at various positions within the cell. Our experimental results and modeling of the mechanical response of the network revealed that bundles were fully embedded along their entire length in a continuous and contractile network of cortical filaments. Moreover, the propagation of the contraction of these bundles throughout the entire cell was dependent on this embedding. In addition, these bundles appeared to originate from the alignment and coalescence of thin and unattached cortical actin filaments from the surrounding mesh.

At the onset of cell locomotion, cells break symmetry to form well-defined cell fronts and rears through the process of cellular polarization. Using an in silico approach, we have identified one of the simplest quantitative frameworks as a possible mechanochemical mechanism for spontaneous cell polarization.