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. 2021 Mar 17;11:6095. doi: 10.1038/s41598-021-85624-5

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Silencing of Is86 fails to interfere with B. burgdorferi persistence in ticks and spirochete transmission. (A) Schematic representation of the full open reading frame of Is86-1 and Is86-2, showing regions targeted for RNA interference. The regions encompassing dsRNA constructs (red arrows) and detection primers that contain common sequences in both Is86-1 and Is86-2 (green) are shown. (B) RNAi induced a significant knockdown of Is86 transcripts (****p < 0.0001). The levels of Is86 gene transcripts in ticks that had been microinjected with pooled dsRNAs targeting Is86-1 and Is86-2 were significantly decreased compared to the dsGFP RNA control. (C) Silencing of Is86 did not affect spirochete persistence in ticks. Spirochete burdens in fully replete ticks were assessed using qPCR and normalizing against tick β-actin. (D) Silencing of Is86 did not block B. burgdorferi transmission from ticks. Spirochete burdens in murine skin were assessed using qPCR. The bars represent the mean ± SEM of four qPCR analyses of B. burgdorferi levels, derived from two independent animal experiments.