GSE169293
Tick Adiponectin Receptor-Mediated Phospholipid Metabolism Contributes to   Borrelia burgdorferi Colonization
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. Overall design: (1)  Tick gut global gene expression change after silencing adiponectin receptor Examination of tick gut response by silencing adiponectin receptor after engorgement on Borrelia burgdorferi-infected or uninfected mice, using RNA-seq (2)  Tick gut global gene expression change after injecting recombinant GFP and adiponectin protein Examination of tick gut response after injecting recombinant GFP and adiponectin protein, using RNA-seq