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. 2018 Jul 30;8:11409. doi: 10.1038/s41598-018-29654-6

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© The Author(s) 2018

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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Model showing A. phagocytophilum mediated AP-1-IAFGP signaling in tick cold tolerance. (A) Upon infection, A. phagocytophilum (shown as morulae within a tick cell) and cold shock upregulate ap-1 gene expression leading to increased production of AP-1 protein. (B) Increased production of AP-1 promotes A. phagocytophilum survival in ticks. In addition, AP-1 translocates into the nucleus and binds to iafgp promoter (C) to increase tick antifreeze gene expression leading to increased production of IAFGP (D) protein. (E) Increased production of IAFGP protects A. phagocytophilum and tick cells from cold. Schematic representation is not to the scale.