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. 2022 Jun 30;13:3776. doi: 10.1038/s41467-022-31455-5

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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. 5 — A Diagram of the KL116 capsule locus identified in strains TP1, TP2, and TP3 as predicted by Kaptive. Genes are represented by arrows oriented in the direction of transcription. Orange arrows represent genes involved in capsule export, yellow genes are involved in repeat unit processing, blue genes are involved in simple sugar biosynthesis, green genes encode glycotransferases and the red gene codes for the initiating transferase. All genes had 100% coverage and ranged from 90–100% identity to the KL116 type in the Kaptive database. Defective capsule locus genes identified in in vitro-generated phage-insensitive mutants of TP1 are indicated by black arrows; numbers in parentheses after each phage name indicate what proportion of phage-insensitive mutants contained a mutation in that gene. B Nucleotide alignment of the sequences showing the six nucleotide deletion in one of the glycosyltransferases (gtr76) found in multiple TP1 mutants resistant to the cocktail myophages.