Abstract
BackgroundTick selenoproteins are involved in regulating oxidative and endoplasmic reticulum stress during prolonged tick feeding on mammalian hosts. How selenoproteins are activated upon tick-borne pathogen infection is yet to be defined.MethodsTo examine the functional role of selenoprotein K in Borrelia burgdorferi infection within the tick host Ixodes scapularis, RNA interference (RNAi)-based gene silencing was performed.ResultsSelenoprotein K is an endoplasmic reticulum (ER)-resident protein and a component of the ERAD complex involved in ER homeostasis. A qRT-PCR assay revealed the significant upregulation of selenogene K (selenoK) expression in B. burgdorferi-infected tick tissues. Silencing of the selenoK transcript significantly depleted B. burgdorferi copies within the infected tick tissues. Upon selenoK knockdown, another component of the ERAD complex, selenoprotein S (selenoS), was significantly upregulated, suggesting a compensatory mechanism to maintain ER homeostasis within the tick tissues. Knockdown of selenoK also upregulated ER stress-related unfolded protein response (UPR) pathway components, ATF6 and EIF2.ConclusionsThe exact mechanisms that contribute to depletion of B. burgdorferi upon selenoK knockdown is yet to be determined, but this study suggests that selenoK may play a vital role in the survival of B. burgdorferi within the tick host.
Highlights
Tick selenoproteins are involved in regulating oxidative and endoplasmic reticulum stress during prolonged tick feeding on mammalian hosts
I. scapularis contains most of the selenogenes which have already been characterized in A. maculatum [5,6,7, 9, 10]
Our data provide a deeper insight into the possible role of selenogene K (selenoK) in the pathogen colonization of tick vectors
Summary
Tick selenoproteins are involved in regulating oxidative and endoplasmic reticulum stress during prolonged tick feeding on mammalian hosts. How selenoproteins are activated upon tick-borne pathogen infection is yet to be defined. In the USA, reported vector-borne diseases are predominantly tick-borne; for example, there are approximately 329,000 cases of Lyme disease annually in the USA. Tick blood-feeding generates toxic levels of reactive oxygen species (ROS) that could damage lipids, proteins and DNA, and promote mutation, cellular dysfunction and cell death. Our previously published studies have shown an adaptive coevolutionary process that has enabled tick-borne pathogen survival by manipulating an antioxidant defense system associated with selenium including a full set of selenoproteins and other antioxidants [3,4,5,6,7,8,9,10,11,12]. Generation of ROS is among the first lines of host defense against invading microbes [13, 14]
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