A swarm of simple active particles confined in a flexible scaffold is a promising system to make mobile and deformable superstructures. These soft structures can perform tasks that are difficult to carry out for monolithic robots because they can infiltrate narrow spaces, smaller than their size, and move around obstacles. To achieve such tasks, the origin of the forces the superstructures develop, how they can be guided, and the effects of external environment, especially geometry and the presence of obstacles, need to be understood. Here, we report measurements of the forces developed by such superstructures, enclosing a number of mindless active rod-like robots, as well as the forces exerted by these structures to achieve a simple function, crossing a constriction. We relate these forces to the self-organization of the individual entities. Furthermore, and based on a physical understanding of what controls the mobility of these superstructures and the role of geometry in such a process, we devise a simple strategy where the environment can be designed to bias the mobility of the superstructure, giving rise to directional motion. Simple tasks—such as pulling a load, moving through an obstacle course, or cleaning up an arena—are demonstrated. Rudimentary control of the superstructures using light is also proposed. The results are of relevance to the making of robust flexible superstructures with nontrivial space exploration properties out of a swarm of simpler and cheaper robots.
Motility is a crucial activity of immune cells allowing them to patrol tissues as they differentiate, sample or exchange information, and execute their effector functions. Although all immune cells are highly migratory, each subset is endowed with very distinct motility patterns in accordance with functional specification. Furthermore individual immune cell subsets adapt their motility behaviour to the surrounding tissue environment. This review focuses on how the generation and adaptation of diversified motility patterns in immune cells is sustained by actin cytoskeleton dynamics. In particular, we review the knowledge gained through the study of inborn errors of immunity (IEI) related to actin defects. Such pathologies are unique models that help us to uncover the contribution of individual actin regulators to the migration of immune cells in the context of their development and function.
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