Vitellogenin-2 Accumulation in the Fat Body and Hemolymph of Babesia -Infected Haemaphysalis longicornis Ticks.

The protozoan parasite spp. invades into tick oocytes and remains in the offspring. The transovarial transmission phenomenon of in ticks has been demonstrated experimentally, but the molecular mechanisms remain unclear. invasion into oocytes occurs along with the progression of oogenesis. In the present study, to find the key tick factor(s) for transmission, we focused on molecules involved in yolk protein precursor (vitellogenin, Vg) synthesis and Vg uptake, which are crucial events in tick oogenesis. With a tick- experimental model, the expression profiles of , , , , and , Vg synthesis-related genes, and Vg receptor () and autophagy-related gene 6 (), Vg uptake-related genes, were analyzed using real-time PCR using tissues collected during the preovipositional period in -infected ticks. The expression levels of () and decreased in the fat body of -infected ticks 1 day after engorgement. In the ovary, mRNA expression was significantly higher in -infected ticks than in uninfected ticks 1 and 2 days after engorgement and decreased 3 days after engorgement. expression was significantly lower in -infected ticks than in uninfected ticks 2 and 4 days after engorgement. had a lower gene expression in -infected ticks compared to uninfected ticks 2 days after engorgement. Additionally, western blot analysis using protein extracts from each collected tissue revealed that Vg-2 (HlVg-2) accumulate in the fat body and hemolymph of -infected ticks. These results suggest that Vg uptake from the hemolymph to the ovary was suppressed in the presence of . Moreover, knockdown ticks had a lower detection rate of DNA in the ovary and a significant reduction of DNA in the hemolymph compared with control ticks. Taken together, our results suggest that accumulated HlVg-2 is associated with infection or transmission in the tick body. These findings, besides previous reports on VgR, provide important information to elucidate the transovarial transmission mechanisms of pathogens in tick vectors.