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. 2017 Jun 9;7:3161. doi: 10.1038/s41598-017-03552-9

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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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ModA2-mediated regulation of H₂O₂ resistance is independent of OxyR. Mutants that lacked oxyR, had significantly decreased survival when exposed to H₂O₂ stress compared to either parent. In contrast to the parents, there was no significant difference in survival between the oxyR mutants themselves. There was no significant difference between the survival of the ΔkatA modA2 locked ON and the ΔkatA modA2 locked OFF mutants, and the survival of both ΔkatA mutants was similar to that of the modA2 locked ON parent. Statistical differences were determined by 1-way ANOVA with Tukey’s multiple comparisons; lines above bars indicate significance, Alpha = 0.05.