Pharmacological Inhibition of the Vacuolar ATPase in Bloodstream-Form Trypanosoma brucei Rescues Genetic Knockdown of Mitochondrial Gene Expression

Claudia Schaffner-Barbero, Migla Miskinyte, Jaspreet Singh Grewal, Achim Schnaufer

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Number of pages7
JournalAntimicrobial Agents and Chemotherapy
Volume62
Issue number9
Early online date18 Jun 2018
DOIs
Publication statusPublished - 27 Aug 2018

Keywords

  • F1Fo-ATPase
  • RNA editing
  • Trypanosoma
  • V-ATPase
  • bafilomycin
  • kDNA
  • kinetoplast
  • mitochondria
  • vacuoles

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