Pharmacological inhibition of the vacuolar ATPase in bloodstream form Trypanosoma brucei rescues genetic knockdown of mitochondrial gene expression [PublishAheadOfPrint]

Trypanosomatid parasites cause diseases in humans and livestock. It was reported that partial inhibition of the vacuolar ATPase (V-ATPase) affects dependence of Trypanosoma brucei on its mitochondrial genome (kDNA), a target of the anti-trypanosomatid drug isometamidium. Here we report that V-ATPase inhibition with bafilomycin A1 (BafA) provides partial resistance to genetic knockdown of mitochondrial gene expression. BafA does not promote long-term survival after kDNA loss, but in its presence, isometamidium causes less damage to kDNA.

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