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.
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