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. 2022 Apr 7;13:1888. doi: 10.1038/s41467-022-29493-0

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© The Author(s) 2022

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–b Transcription analysis of msrC in pleuromutilin-sensitive VRE_fm CAU369 (a) and pleuromutilin-resistant VRE_fm CAU378 (b). c Proteomics analysis of VRE_fm CAU378 treated with 1× and 10 × MIC lefamulin for 1 h. Proteins were identified as significantly different with fold changes of log₂ [fold changes] values of at fold-increase or fold-decrease of expression levels. d Comparison of lefamulin binding sites within the MsrC-ribosome complex. The 50S (green) and 30S (gray) subunits (PDB 5AA0 [https://www.rcsb.org/structure/5AA0]), and the A-site tRNA (purple) and P-site tRNA (blue) are shown. Binding of MsrC (red, homology of the template with PDB 5ZLU [https://www.rcsb.org/structure/5ZLU], middle) blocks the binding of lefamulin (brick-red, PDB 5HL7 [https://www.rcsb.org/structure/5HL7], right) to PTC in the 50S subunit. Data were presented as means ± S.D. n.s., not significant, determined by non-parametric one-way ANOVA (n = 3).