Edge current and pairing order transition in chiral bacterial vortices

Bacterial suspensions show turbulence-like spatiotemporal dynamics and vortices moving irregularly inside the suspensions. Understanding these ordered vortices is an ongoing challenge in active matter physics, and their application to the control of autonomous material transport will provide significant development in microfluidics. Despite the extensive studies, one of the key aspects of bacterial propulsion has remained elusive: The motion of bacteria is chiral, i.e., it breaks mirror symmetry. Therefore, the mechanism of control of macroscopic active turbulence by microscopic chirality is still poorly understood. Here, we report the selective stabilization of chiral rotational direction of bacterial vortices in achiral circular microwells sealed by an oil/water interface. The intrinsic chirality of bacterial swimming near the top and bottom interfaces generates chiral collective motions of bacteria at the lateral boundary of the microwell that are opposite in directions. These edge currents grow stronger as bacterial density increases, and, within different top and bottom interfaces, their competition leads to a global rotation of the bacterial suspension in a favored direction, breaking the mirror symmetry of the system. We further demonstrate that chiral edge current favors corotational configurations of interacting vortices, enhancing their ordering. The intrinsic chirality of bacteria is a key feature of the pairing order transition from active turbulence, and the geometric rule of pairing order transition may shed light on the strategy for designing chiral active matter.

Phenomenological model of bacterial aerotaxis with a negative feedback

A phenomenological model for the suspension of the aerotactic swimming microorganisms placed in a chamber with its upper surface open to air is presented. The model was constructed to embody some complexity of the aerotaxis phenomenon, especially, changes in the average bacteria drift velocity under changing environmental conditions. It was assumed that effective forces applied to the cell (gravitational, drag, and thrust) should be essential for the overall system dynamics; and that bacterial propulsion force, but not their swimming velocity, is proportional to the gradient of the oxygen concentration. Mathematically, the model consists of three coupled equations for the oxygen dynamics; for the cell conservation; and for the balance of forces acting on bacteria. An analytical steady-state solution is given for the shallow and deep layers and numerical results are given for the steady-state and initial value problems which are compared with corresponding ones to the Keller–Segel model.

Adapter Protein SH2-Bβ Stimulates Actin-Based Motility of Listeria monocytogenes in a Vasodilator-Stimulated Phosphoprotein (VASP)-Dependent Fashion

ABSTRACT SH2-Bβ (Src homology 2 Bβ) is an adapter protein that is required for maximal growth hormone-dependent actin reorganization in membrane ruffling and cell motility. Here we show that SH2-Bβ is also required for maximal actin-based motility of Listeria monocytogenes. SH2-Bβ localizes to Listeria-induced actin tails and increases the rate of bacterial propulsion in infected cells and in cell extracts. Furthermore, Listeria motility is decreased in mouse embryo fibroblasts from SH2-B−/− mice. Both recruitment of SH2-Bβ to Listeria and SH2-Bβ stimulation of actin-based propulsion require the vasodilator-stimulated phosphoprotein (VASP), which binds ActA at the surfaces of Listeria cells and enhances bacterial actin-based motility. SH2-Bβ enhances actin-based movement of ActA-coated beads in a biomimetic actin-based motility assay, provided that VASP is present. In vitro binding assays show that SH2-Bβ binds ActA but not VASP; however, binding to ActA is greater in the presence of VASP. Because VASP also plays an essential regulatory role in actin-based processes in eukaryotic cells, the present results provide mechanistic insight into the functions of both SH2-Bβ and VASP in motility and also increase our understanding of the fundamental mechanism by which Listeria spreads.