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. 2017 Sep 15;7:11734. doi: 10.1038/s41598-017-11967-7

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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LuxR-3OC6-HSL represses a P_ainS -gfp reporter. Both panels report fluorescence of cells harboring P_ainS -gfp reporter pHK12 grown in SWTO to an OD₅₉₅ of ~2.5. Strains harboring the reporter lack AHL synthases (∆luxI ∆ainS) and feedback regulation of luxR (litR::ermR P_con -luxR), and either express luxR ^ES114 (JHK045), luxR ^MJ1 (JHK099), or no luxR (JHK046). Panel A: Strains with luxR ^ES114 (grey bars) or no luxR (white bars) harboring pHK12 and supplemented with 500 nM 3OC6-HSL and/or C8-HSL. Treatments marked with different letters are significantly different (P < 0.05) as determined by one-way ANOVA. Panel B: Strains with luxR ^ES114 or luxR ^MJ1, carrying pHK12, in media with varied 3OC6-HSL concentrations. In both panels, bars indicate standard error (n = 3).