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• W2069995177 abstract "The widespread use of antibiotics and the emergence of resistant strains call for new approaches to treat bacterial infection. Bacterial cell−cell communication or “quorum sensing” (QS) is mediated by “signatures” of small molecules that represent targets for “quenching” communication and avoiding virulent phenotypes. Only a handful of small molecules that antagonize the action of the “universal” autoinducer, AI-2, have been reported. The biological basis of antagonism, as well as the targets for these select few AI-2 antagonists, have not been clearly defined. We have developed C-1 alkyl analogs of AI-2 that quench the QS response in multiple bacterial species simultaneously. We also demonstrate the biological basis for this action. Like AI-2, the analogs are activated by the bacterial kinase, LsrK, and modulate AI-2 specific gene transcription through the transcriptional regulator, LsrR. Interestingly, addition of a single carbon to the C1-alkyl chain of the analog plays a crucial role in determining the effect of the analog on the QS response. While an ethyl modified analog is an agonist, propyl becomes an antagonist of the QS circuit. In a trispecies synthetic ecosystem comprised of E. coli, S. typhimurium, and V. harveyi we discovered both cross-species and species-specific anti-AI-2 QS activities. Our results suggest entirely new modalities for interrupting or tailoring the network of communication among bacteria." @default.
• W2069995177 created "2016-06-24" @default.
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• W2069995177 date "2010-07-26" @default.
• W2069995177 modified "2023-10-07" @default.
• W2069995177 title "Synthetic Analogs Tailor Native AI-2 Signaling Across Bacterial Species" @default.
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• W2069995177 doi "https://doi.org/10.1021/ja102587w" @default.
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