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. 2019 May 28;5:29. doi: 10.1038/s41421-019-0101-2

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© The Author(s) 2019

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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Fig. 3 — a DNA-binding activities of wild-type AimR and AimR mutants were examined. The AimR concentrations in lanes 1–5 were 0, 0.008, 0.04, 0.2, and 1 μM, respectively. The concentration of the 31 bp DNA fragment was 20 nM. The arbitrium peptide (GMPRGA) and an unrelated peptide (GFGHGA) were added as controls. AimR–DNA complex is indicated by a black arrowhead, and free DNA is indicated by a black asterisk. b Effect of AimR mutations on the infection dynamics of SPbeta. Growth curves of B. subtilis strain CU1065 infected with SPbeta, or that of B. subtilis strain CU1065 (amyE::aimR WT, K29D, N30A, N32A, K43D, T44D, N46D, K77D, T78D, K79D, R82D, N109D, K145D, or K120D) infected with SPbeta ΔaimR at MOI = 0.001. Data represent an average of three biological replicates, and each with three technical replicates. Error bars indicate the s.d. of at least three independent measurements (the points are the mean)