title: Signaling-mediated bacterial persister formation.
abstract: 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 subpopulation against antibiotics by activating stress responses, leading to persister formation.
authors.affiliation: Howard Hughes Medical Institute, Boston University, Boston, Massachusetts, USA.
authors.forename: Nicole M
authors.initials: NM
authors.lastname: Vega
authors.forename: Kyle R
authors.initials: KR
authors.lastname: Allison
authors.forename: Ahmad S
authors.initials: AS
authors.lastname: Khalil
authors.forename: James J
authors.initials: JJ
authors.lastname: Collins
mesh_terms: D024881:Drug Resistance, Bacterial; D004926:Escherichia coli / Q000378:metabolism / Q000502:physiology*; D029968:Escherichia coli Proteins / Q000378:metabolism; D007211:Indoles / Q000378:metabolism*; D044085:Microfluidics; D018384:Oxidative Stress; D012097:Repressor Proteins / Q000378:metabolism; D015398:Signal Transduction; D013312:Stress, Physiological
chemical_list: D029968:Escherichia coli Proteins; D007211:Indoles; D012097:Repressor Proteins; C499299:oxyR protein, E coli