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. 2019 Mar 12;10:1177. doi: 10.1038/s41467-019-09058-4

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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. 4 — Resistance enhancement involves RecA, SOS induction, and UmuDC. a OFL persisters derived from ΔrecA (n = 3), which is defective in SOS induction and recombinatorial repair, do not give rise to a population with increased RIF resistance. Complementation of ΔrecA restores the enhancement of RIF-resistant mutants from OFL persisters (n = 6), whereas persisters from ΔrecA mutants bearing the pBAD33 control do not give rise to a population with enhanced RIF resistance (n = 8). b Increase in RIF-resistant mutants was not observed in OFL persisters derived from lexA3 mutants (n = 4), which cannot induce SOS. c Upon deleting umuDC, which encodes error-prone, SOS-induced DNA polymerase V, a significant increase in RIF-resistant mutants in OFL persister-derived populations was observed (n = 5), but the magnitude of that increase was significantly lower than that of wild-type (n = 13). Mutants lacking error-prone polymerase II (ΔpolB, n = 6) or error-prone polymerase IV (ΔdinB, n = 6) had significant increases in RIF-resistant mutants in OFL persister-derived populations that were of a comparable magnitude as wild-type. d Complementation of UmuDC on pBAD33 in ΔumuDC mutants restores increase in RIF-resistant colonies from OFL persisters (n = 7), whereas the presence of pBAD33 control fails to restore the phenotype (n = 9). Error bars portray S.E.M. * indicates significance (p ≤ 0.05) between log-transformed fold-changes and log-transformed value of 1 (fold-change of 1 would indicate no difference in resistant mutants). # indicates significance (p ≤ 0.05, using two-tailed t-tests with unequal variances) between log-transformed fold-changes and those of wild-type. Zero values for ΔrecA+pBAD33 were not included in the statistical analysis because they could not be log-transformed