Nonequilibrium statistical physics of biological function: a reappraisal of cooperative sensing in bacterial chemotaxis

Living systems spend energy to enhance a variety of biological functions, from growth and assembly to transport and environmental sensing. For example, bacteria sense and respond to chemical stimuli (e.g. nutrients or toxins) via the chemotaxis signaling pathway, whose information transmission is powered by continuous energy dissipation from ATP hydrolysis. While existing theories predominantly describe signaling response with equilibrium models, recent experiments reveal subtle new signatures of the nonequilibrium dynamics underlying the chemosensory array: (1) adaptive shifts in downstream signaling response are disproportionately larger than shifts in ligand binding response and (2) cells spontaneously switch between active and inactive signaling states, with dynamics that break time-reversal symmetry. In this talk, I will introduce nonequilibrium allosteric and lattice models of the chemosensory array that incorporate dissipative chemical reaction cycles with cooperative interactions between receptor functional units. Our models not only resolve the two puzzles in experimental measurements but also provide insight into the general mechanisms governing dissipation-enhanced adaptive sensing in biological systems. By operating far from equilibrium, cells amplify their adaptive range and ease a speed-sensitivity trade-off to simultaneously achieve both sensitive and rapid signaling response.