For most organisms, iron is an essential nutrient due to its role in fundamental cellular processes. Insufficient iron causes sub-optimal metabolism with potential effects on viability, while high levels of iron are toxic due to the formation of oxidative radicals, which damage cellular components. Many molecules and processes employed in iron uptake, storage, transport and metabolism are conserved, however significant knowledge gaps remain regarding these processes in ticks due to their unique physiology. In this study, we first identified and sequenced 13 genes likely to be involved in iron metabolism in Dermacentor andersoni cells. We then developed a method to reduce iron levels in D. andersoni cells using the iron chelator 2,2'-bipyridyl and measured the transcriptional response of these genes to iron reduction. The genes include a putative transferrin receptor, divalent metal transporter 1, duodenal cytochrome b, zinc/iron transporters zip7, zip13, zip14, mitoferrin, ferrochelatase, iron regulatory protein 1, ferritin1, ferritin2, transferrin and poly r(C)-binding protein. Overall, the transcriptional response of the target genes to iron reduction was modest. The most marked changes were a decrease in ferritin2, which transports iron through the tick hemolymph, the mitochondrial iron transporter mitoferrin, and the mitochondrial enzyme ferrochelatase. Iron regulatory protein1 was the only gene with an overall increase in transcript in response to reduced iron levels. This work lays the foundation for an improved understanding of iron metabolism in ticks which may provide molecular targets for the development of novel tick control methods and aid in the understanding of tick-pathogen interactions.
Keywords: 2, 2′-bipyridyl; Dermacentor spp.; Iron metabolism; Iron reduction; Tick physiology.
Published by Elsevier GmbH.