Extensile actomyosin?

Living cells move thanks to assemblies of actin filaments and myosin motors that range from very organized striated muscle tissue to disordered intracellular bundles. The mechanisms powering these disordered structures are debated, and all models studied so far predict that they are contractile. We reexamine this prediction through a theoretical treatment of the interplay of three well-characterized internal dynamical processes in actomyosin bundles: actin treadmilling, the attachement-detachment dynamics of myosin and that of crosslinking proteins. We show that these processes enable an extensive control of the bundle's active mechanics, including reversals of the filaments' apparent velocities and the possibility of generating extension instead of contraction. These effects offer a new perspective on well-studied in vivo systems, as well as a robust criterion to experimentally elucidate the underpinnings of actomyosin activity.Comment: 5 pages, 5 figure

Connecting local active forces to macroscopic stress in elastic media

In contrast with ordinary materials, living matter drives its own motion by generating active, out-of-equilibrium internal stresses. These stresses typically originate from localized active elements embedded in an elastic medium, such as molecular motors inside the cell or contractile cells in a tissue. While many large-scale phenomenological theories of such active media have been developed, a systematic understanding of the emergence of stress from the local force-generating elements is lacking. In this paper, we present a rigorous theoretical framework to study this relationship. We show that the medium's macroscopic active stress tensor is equal to the active elements' force dipole tensor per unit volume in both continuum and discrete linear homogeneous media of arbitrary geometries. This relationship is conserved on average in the presence of disorder, but can be violated in nonlinear elastic media. Such effects can lead to either a reinforcement or an attenuation of the active stresses, giving us a glimpse of the ways in which nature might harness microscopic forces to create active materials.Comment: 9 pages, 4 figure

Geometrical frustration yields fiber formation in self-assembly

Controlling the self-assembly of supramolecular structures is vital for living cells, and a central challenge for engineering at the nano- and microscales. Nevertheless, even particles without optimized shapes can robustly form well-defined morphologies. This is the case in numerous medical conditions where normally soluble proteins aggregate into fibers. Beyond the diversity of molecular mechanisms involved, we propose that fibers generically arise from the aggregation of irregular particles with short-range interactions. Using a minimal model of ill-fitting, sticky particles, we demonstrate robust fiber formation for a variety of particle shapes and aggregation conditions. Geometrical frustration plays a crucial role in this process, and accounts for the range of parameters in which fibers form as well as for their metastable character.Comment: 6 pages, 5 figures, 1 ancillary movie; to appear in Nature Physic

Fiber networks amplify active stress

Large-scale force generation is essential for biological functions such as cell motility, embryonic development, and muscle contraction. In these processes, forces generated at the molecular level by motor proteins are transmitted by disordered fiber networks, resulting in large-scale active stresses. While these fiber networks are well characterized macroscopically, this stress generation by microscopic active units is not well understood. Here we theoretically study force transmission in these networks, and find that local active forces are rectified towards isotropic contraction and strongly amplified as fibers collectively buckle in the vicinity of the active units. This stress amplification is reinforced by the networks' disordered nature, but saturates for high densities of active units. Our predictions are quantitatively consistent with experiments on reconstituted tissues and actomyosin networks, and shed light on the role of the network microstructure in shaping active stresses in cells and tissue.Comment: 8 pages, 4 figures. Supporting information: 5 pages, 5 figure

On the microstructure of active cellular processes

Eukaryotic cells use a multitude of protein machines to regulate their own structure. In this thesis, we study how the geometrical arrangement of these interacting microscopic active elements sculpt the cell's own internal microstructure and its membrane enclosure.We first focus on the mechanisms generating actomyosin contractility, a crucial driver of cell motion and organization. We question the current position of highly organized, sarcomeric contractility as the only possible mechanism to drive contractility. We propose an alternative mechanism, and show that only it can account for the observed contractility of disordered actomyosin assemblies. It moreover yields qualitatively new effects in intracellular force transmission, including stress reversal and amplification, consistent with experimentally observations in fiber networks.We next elucidate some of the mechanisms through which the cell deforms and cuts its own membrane, thus enabling exchanges with the extracellular medium as well as between its internal compartments. We find that the function of the proteins responsible for this remodeling is strongly influenced by the mechanics of the membrane, and use these effects to elucidate the modes of operation of proteins clathrin and dynamin, as well as of protein complex ESCRT-III

Psychological pressure in competitive environments: Evidence from a randomized natural experiment: Comment

Apesteguia and Palacios-Huerta (forthcoming) report for a sample of 129 shootouts from various seasons in ten different competitions that teams kicking first in soccer penalty shootouts win significantly more often than teams kicking second. Collecting data for the entire history of six major soccer competitions we cannot replicate their result. Teams kicking first win only 53.4% of 262 shootouts in our data, which is not significantly different from random. Our findings have two implications: (1) Apesteguia and Palacios-Huerta’s results are not generally robust. (2) Using specific subsamples without a coherent criterion for data selection might lead to non-representative findings