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. 2021 Aug 26;12:5145. doi: 10.1038/s41467-021-25484-9

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© The Author(s) 2021

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 — Midpoint rooted maximum-likelihood phylogeny of 116 members of clone A3. Each evolutionary gain or loss of a drug resistance mutation was assigned to its position on the phylogeny using parsimony. Given its basilar position on the phylogeny, the T28C erm(41) variant (blue circle), which precludes inducible macrolide resistance, occurred earlier in time, with subsequent-independent reversions back to T28 (red circles), indicating a regain of the inducible macrolide resistance phenotype. Within the clade, additional acquisitions of constitutive macrolide and amikacin resistance were also observed, with emergence of rrl A2270C (E. coli A2058C), rrl A2270G (E. coli A2058G), rrl A2271C (E. coli A2059C), rrl A2271G (E. coli A2059G), and rrs A1374G (E. coli A1408G). Bootstrap values (≥80%) support the independent, convergent acquisition of each instance of macrolide and amikacin resistance.