Molecular basis of resistance to cytochrome bc1 inhibitors

FEMS Yeast Res. 2008 Mar;8(2):183-92. doi: 10.1111/j.1567-1364.2007.00328.x. Epub 2007 Dec 17.

Abstract

Inhibitors of the mitochondrial respiratory chain enzyme cytochrome bc1 (respiratory complex III) have been developed as antimicrobial agents. They are used in agriculture to control plant pathogenic fungi and in medicine against human pathogens, such as the malaria parasite Plasmodium falciparum, or Pneumocystis jiroveci (an opportunistic pathogenic fungus life-threatening in immuno-compromised patients). These respiratory inhibitors are thus effective against a broad range of important pathogens. Unfortunately, the problem of acquired resistance has rapidly emerged. A growing number of pathogen isolates resistant to inhibitor treatment have been reported, and this resistance is often linked to mutation within cytochrome b, one of the essential catalytic subunits of the complex. Saccharomyces cerevisiae is an invaluable model in order to assess the impact of the mutations on the sensitivity to the drugs, on the respiratory capacity and the fitness of cells. In this minireview, the inhibitors, their mode of action, and the mutations implicated in resistance and studied in yeast are briefly reviewed. Four mutations that are of particular importance in medicine and in agriculture are briefly reviewed and described in more detail and the molecular basis of resistance and of evolution of the mutations is discussed succinctly.

Publication types

  • Review

MeSH terms

  • Animals
  • Anti-Infective Agents / pharmacology*
  • Drug Resistance, Microbial*
  • Electron Transport Complex III / antagonists & inhibitors*
  • Eukaryota / drug effects*
  • Fungi / drug effects*
  • Humans

Substances

  • Anti-Infective Agents
  • Electron Transport Complex III