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The exact mechanisms that contribute to
depletion of B. burgdorferi upon
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.***
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.