Signalingmediated bacterial persister formation

Here we show that bacterial communication through indole signaling induces persistence, a phenomenon in which a subset of an isogenic bacterial population tolerates antibiotic treatment. We monitor indole-induced persister formation using microfluidics, and identify the role of oxidative stress and phage-shock pathways in this phenomenon. We propose a model in which indole signaling “inoculates ” a bacterial sub-population against antibiotics by activating stress responses, leading to persister formation. Bacterial persisters are dormant cells1 within an isogenic bacterial population that tolerate antibiotic treatment2 and have been implicated in chronic and recurrent infections3–5. Persister formation occurs heterogeneously within an antibiotic-susceptible population, predominantly at the transition to stationary phase6,7. Though numerous genes have been associated with persistence8–10, a complete understanding of persister formation remains elusive. There is increasing evidence that bacterial communication via chemical signaling plays a role in establishing population heterogeneity11. The bacterial stationary phase signalin