Predicted Dermacentor andersoni iron metabolism genes and their response to iron reduction in cultured tick cellsPredicted Dermacentor andersoni iron metabolism genes and their response to iron reduction in cultured tick cells

Primary author: Muna Solyman
Faculty sponsor: Susan M. Noh

Primary college/unit: College of Veterinary Medicine
Campus: Pullman

Abstract:

For most organisms, iron is an essential nutrient due to its role in many cellular processes. Consequently, insufficient iron levels cause cell damage and death while high concentrations of iron are toxic due to the formation of oxidative radicals, which damage cellular components. As obligate hematophagous parasites, ticks have access to large amounts of iron. Unlike all other hematophagous invertebrates, blood meal digestion within ticks occurs intracellularly rather than in the gut lumen. Due to their unique physiology, little is known about iron uptake and regulation in ticks. Some genes have been identified that are hypothesized to be involved in iron metabolism based on the presence of conserved domains and some limited experimental evidence. In this project, thirteen likely iron metabolism genes were chosen based on the literature and bioinformatics. Using, Dermacentor andersoni ticks, which do not have a published genome, we identified and sequenced these genes. Next, we developed a method to reduce iron in cultured tick cells using an iron chelator 2,2′-bipyridyl and measured the transcriptional response of the D. andersoni iron metabolism genes to iron reduction. Overall, the response of tick cells to iron reduction was less marked than in mammalian cells. The iron transport gene, ferritin 2, and the mitochondrial iron transporters ferrochelatase and mitoferrin were down regulated, while iron regulator protein 1 was up-regulated in response to reduced iron levels. This work lays a foundation for an improved understanding of iron metabolism in ticks and the potential identification of anti-tick targets.