Bacteria Hedge Their Bets

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Science  06 Apr 2012:
Vol. 336, Issue 6077, pp. 13
DOI: 10.1126/science.336.6077.13-d

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Antibiotic treatment may be thwarted by bacteria, not only because molecular mechanisms of resistance are acquired and selected, but also because persister cells withstand the onslaught by becoming dormant. We know persister-cell formation occurs as bacterial populations move from log to stationary-phase growth, but little else. Vega et al. have implicated the bacterial signalling molecule indole in the enhancement of persistence to various antibiotic treatments by monitoring the formation of persisters and their transcriptional responses to indole. Gene expression in the oxidative stress regulator and phage-shock pathways increased, but drug efflux systems did not, suggesting that molecular antibiotic resistance pathways were not being induced in these conditions. Knocking out these genes resulted in less persistence. Activation of these responses, via indole signalling induced by low-level antibiotic exposure or other stress, may thus prepare a proportion of the bacterial population for further unpredictable and potentially harmful events—a form of “bet hedging.”

Nat. Chem Biol. 8, 10.1038/nchembio.915 (2012).

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