The Lyme disease agent co-opts adiponectin receptor-mediated signaling in its arthropod vector

eLife

Utpal Pal¹  Xiaotian Tang²  Alejandro Marín-López²  Jesse Hwang²  Sukanya Narasimhan²  Gunjan Arora²  Ming-Jie Wu²  Erol Fikrig²  Yu-Min Chuang²  Andaleeb Sajid²  Yongguo Cao³  Hongwei Ma⁴  Sameet Mehta⁵  Courtney L Brown⁶ 

[1] Department of Veterinary Medicine, University of Maryland, College Park, College Park, United States;Section of Infectious Diseases, Department of Internal Medicine, School of Medicine, Yale University, New Haven, United States;Section of Infectious Diseases, Department of Internal Medicine, School of Medicine, Yale University, New Haven, United States;Department of Clinical Veterinary Medicine, and Key Laboratory for Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun, China;Section of Infectious Diseases, Department of Internal Medicine, School of Medicine, Yale University, New Haven, United States;Department of Microbiology, School of Basic Medicine, Fourth Military Medical University, Shaanxi, China;Yale Center for Genome Analysis, Yale University, New Haven, United States;Yale Combined Program in the Biological and Biomedical Sciences, Yale University, New Haven, United States;

关键词: adiponectin receptor;    Ixodes scapularis;    Borrelia burgdorferi;    Mouse;    Other;   

DOI  :  10.7554/eLife.72568

来源: eLife Sciences Publications, Ltd

【 摘 要 】

Adiponectin-mediated pathways contribute to mammalian homeostasis; however, little is known about adiponectin and adiponectin receptor signaling in arthropods. In this study, we demonstrate that Ixodes scapularis ticks have an adiponectin receptor-like protein (ISARL) but lack adiponectin, suggesting activation by alternative pathways. ISARL expression is significantly upregulated in the tick gut after Borrelia burgdorferi infection, suggesting that ISARL signaling may be co-opted by the Lyme disease agent. Consistent with this, RNA interference (RNAi)-mediated silencing of ISARL significantly reduced the B. burgdorferi burden in the tick. RNA-seq-based transcriptomics and RNAi assays demonstrate that ISARL-mediated phospholipid metabolism by phosphatidylserine synthase I is associated with B. burgdorferi survival. Furthermore, the tick complement C1q-like protein 3 interacts with ISARL, and B. burgdorferi facilitates this process. This study identifies a new tick metabolic pathway that is connected to the life cycle of the Lyme disease spirochete.

【 授权许可】

CC BY