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. 2020 Oct 1;11:4915. doi: 10.1038/s41467-020-18668-2

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© The Author(s) 2020

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. 5 — Schematic of the proposed mechanism of amplification leading to hyperproduction of TEM-1B; (1) a pseudo compound transposon, PTn6762, is present on the chromosome flanked by two copies of IS26. (2) PTn6762 is excised from the chromosome, (3) which then forms a TU which (4) re-inserts into the chromosome adjacent to the chromosomally located IS26 (5) creating a tandem array of the TU and increasing the copy number of bla_TEM-1B.