Net force | EPFL Graph Search

In mechanics, the net force is the sum of all the forces acting on an object. For example, if two forces are acting upon an object in opposite directions, and one force is greater than the other, the forces can be replaced with a single force that is the difference of the greater and smaller force. That force is the net force. When forces act upon an object, they change its acceleration. The net force is the combined effect of all the forces on the object's acceleration, as described by Newton's second law of motion. When the net force is applied at a specific point on an object, the associated torque can be calculated. The sum of the net force and torque is called the resultant force, which causes the object to rotate in the same way as all the forces acting upon it would if they were applied individually. It is possible for all the forces acting upon an object to produce no torque at all. This happens when the net force is applied along the line of action. In some texts, the ter

Dynamics of actin and myosin II during cell polarization and directional locomotion

Sophie Bohnet

Crawling cell motility is characteristic of most animal cells and is involved in many important biological processes such as embryogenesis, immune response, and wound healing. It involves several steps: protrusion (dynamic surface extension) at the front of the cell, attachment to the substratum, and forward translocation of the cell body accompanied by the detachment and retraction of the rear portion of the cell. Crawling motion is believed to be based on actin, a major component of the cytoskeleton, and myosin II, a motor protein that is believed to produce contraction force by moving along actin filaments. Actin and myosin II are the two major structural and force-generating components of the cell's motile machinery. Protrusion is thought to be driven by the assembly of a dense actin network that is attached to the substrate through integrin-containing adhesions. Previous studies estimated the forces generated by actin polymerization and the adhesion forces, but the net force developed by the protruding leading edge has not been yet determined. The forward translocation of the cell body is believed to depend on the interaction of myosin with the actin network, but the exact mechanisms behind this interaction are still unclear. Moreover, it is still poorly understood how the molecular reactions involved in each step of the crawling motion are coordinated to result in the integrated cellular response. In this thesis work, we have quantitatively characterized the assembly and motion of actin and myosin II in the stationary and migratory states of the cell, and during the transition between these two steady-states. We have also measured the force developed by the protruding leading edge. The experimental system used is the fish epidermal keratocytes, one of the most spectacular models of cell locomotion. These cells are characterized by fast and persistent migration, and a stable and simple cytoskeletal organization. Enhanced phase contrast, interference reflection, classical fluorescence and fluorescent speckles microscopy were used as imaging techniques along with computer-based tracking approaches. We have first studied actin movement and assembly in the lamellipodium of keratocyte (thin, sheet-like extension at the leading edge of the cell). Actin dynamics in the lamellipodia of many cell types are characterized by retrograde flow of the actin network away from the leading edge. This flow is believed to result from membrane resistance to actin assembly and contractile forces in the network, and was speculated to play a role in controlling the cell shape and motion. Retrograde flow was previously observed in every crawling cell with the exception of keratocytes. We have for the first time detected actin retrograde flow throughout the keratocyte lamellipodium at velocities of 1–3 µm/min and analyzed its organization and relation to the cell motion during both unobstructed persistent migration and events of cell collision. We have found that freely moving cells exhibited a graded flow velocity increasing toward the sides of the lamellipodium, whereas in colliding cells, the velocity decreased markedly at the site of collision, with striking alteration of the flow in other lamellipodial regions. Our findings support the universality of the flow phenomenon and indicate that maintenance of the keratocyte shape during locomotion depends on the regulation of retrograde flow and actin polymerization. We have subsequently quantitatively characterized the assembly and movement of actin and myosin II throughout the entire keratocyte. Actin exhibited a slow backward motion in the lamellipodium and a faster forward motion in the trailing cell body. The change of direction occurred along the line parallel to the leading edge of the cell just in front of the front boundary of the cell body. Myosin II also moved forward in the cell body, but no motion with respect to the substratum was detected in the lamellipodium. At the cell sides, actin and myosin II exhibited motion towards the cell center with velocities increasing with the distance from the center. Net assembly of actin occurred locally at the leading edge of the lamellipodium, and disassembly at the back of the lamellipodium. Myosin II assembled in a distributed manner in the lamellipodium and disassembled in the cell body. Eventually, a simultaneous tracking of actin and myosin II revealed that myosin II moved forward relatively to actin throughout the cell. Taken together, these results suggest a longitudinal and transverse contraction along the lamellipodium/cell body junction. To understand how the polarized patterns of the organization of actin/myosin machinery were first established, we have studied in the next part of the work random cell polarization, i.e. the spontaneous transition between the stationary and the migratory state of a cell in the absence of external directional stimuli. Cell polarization and directional locomotion are believed to involve asymmetry in actin assembly, contractility, and substrate adhesion. We have analyzed the distribution and dynamics of actin and myosin II and the dynamics of substrate adhesions during cell polarization. In the stationary state, the cells exhibited lamellipodia with a uniform rate of actin retrograde flow all around the cell perimeter. Upon initiation of directional movement, retrograde flow accelerated at the prospective rear of the cell, but the lamellipodia initially persisted all around the perimeter. The assembly of actin network also continued all around the cell. Local areas of detachment from the substrate were observed at the base of rear lamellipodia. Treatment with myosin inhibitor blebbistatin nearly completely blocked the polarization. Depolymerization of microtubules with nocodazole resulted in attenuated polarization. Taken together, these results suggest that initial polarization results from asymmetry in actin retrograde flow, which is induced by myosin-dependent contraction and stabilized by microtubules. Finally, we have estimated the force necessary to stall the protruding leading edge of the keratocytes. We arrested the leading edge of a moving cell with a hydrodynamic load generated by a fluid flow from a micropipette. The flow arrested the protrusion locally, as the cell approached the pipette, causing an arc-shaped indentation and upward folding of the leading edge. Modeling of the fluid flow gave a surprisingly low value for the arresting force of just a few piconewtons per micrometer. This small force did not abolish actin polymerization nor disrupt the adhesions formed before the arrest, but rather interfered with the weak nascent adhesions at the very front of the cell. We conclude that a weak external force is sufficient to reorient the growing actin network at the leading edge and to stall the cell protrusion. Our study of the dynamics of actin and myosin II in polarizing and migrating cells provides novel and important insights into the cell motility mechanism and establishes a fundamental quantitative data set necessary to test and improve theoretical models of cell motility.

EPFL2006

The dynamics and timescales of static stall

Julien Dominique Claude Deparday, Sébastien Le Fouest, Karen Ann J Mulleners

Airfoil stall plays a central role in the design of safe and efficient lifting surfaces. We typically distinguish between static and dynamic stall based on the unsteady rate of change of an airfoil’s angle of attack. Despite the somewhat misleading denotation, the force and flow development of an airfoil undergoing static stall are highly unsteady and the boundary with dynamic stall is not clearly defined. We experimentally investigate the forces acting on a two-dimensional airfoil that is subjected to two manoeuvres leading to static stall: a slow continuous increase in angle of attack with a reduced pitch rate of 1.3 10−4 and a step-wise increase in angle of attack from 14.2°to 14.8°within 0.04 convective times. We systematically quantify the stall reaction delay, or the timespan between the moment the blade exceeds its critical static stall angle and the onset of stall, for many repetitions of these two manoeuvres. The onset of flow stall is marked by the distinct drop in the lift coefficient. The reaction delay for the slow continuous ramp-up manoeuvre is not influenced by the blade kinematics and its occurrence histogram is normally distributed around 32 convective times. The static reaction delay is compared with dynamic stall delays for dynamic ramp-up motions with reduced pitch rates ranging from 9 10−4 to 0.14 and for dynamic sinusoidal pitching motions of different airfoils at higher Reynolds numbers up to 1 106. The stall delays for all conditions follow the same power law decrease from 32 convective times for the most steady case down to an asymptotic value of 3 convective times for reduced pitch rates above 0.04. Static stall is not phenomenologically different than dynamic stall and is merely a typical case of stall for low pitch rates where the onset of flow separation is not promoted by the blade kinematics. Based on our results, we suggest that conventional measurements of the static stall angle and the static load curves should be conducted using a continuous and uniform ramp-up motion at a reduced frequency around 1 10−4.

2021

Robot-Animal Interaction: Perception and Behavior of Insbot

Masoud Asadpour, Gilles Caprari, Walter Karlen, Roland Siegwart, Fabien Tâche

This paper describes hardware and behavior implementation of a miniature robot in size of a match box that simulates the behavior of cockroaches in order to establish a social interaction with them. The robot is equipped with two micro-processors dedicated to hardware processing and behavior generation. The robot can discriminate cockroaches, other robots, environment boundaries and shelters. It has also three means of communication to monitor, log, supervise the biological experiment, and detect the other robots in short range. The behavioral model of the robot is a mixture of fusion in low-level and arbitration in high-level. In arbitration level a stochastic state machine selects the proper subtask. Then in fusion level, that subtask is decomposed to a hierarchy of sub-tasks. Each sub-task generates a potential field. The resultant force is then mapped to an action.