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Toxoplasma gondii is an apicomplexan parasite that causes fatal and debilitating brain and eye disease. Endochinlike quinolones (ELQs) are preclinical compounds that are efficacious against apicomplexan-caused diseases, including toxoplasmosis, malaria, and babesiosis. Of the ELQs, ELQ-316 has demonstrated the greatest efficacy against acute and chronic experimental toxoplasmosis. Although genetic analyses in other organisms have highlighted the importance of the cytochromebc 1 complex Qi site for ELQ sensitivity, the mechanism of action of ELQs againstT. gondii and the specific mechanism of ELQ-316 remain unknown. Here, we describe the selection and genetic characterization ofT. gondii clones resistant to ELQ-316. AT. gondii strain selected under ELQ-316 drug pressure was found to possess a Thr222-Pro amino acid substitution that confers 49-fold resistance to ELQ-316 and 19-fold resistance to antimycin, a well-characterized Qi site inhibitor. These findings provide further evidence for ELQ Qi site inhibition inT. gondii and greater insight into the interactions of Qi site inhibitors with the apicomplexan cytochromebc 1 complex.

Genetic Evidence for Cytochrome b Q i Site Inhibition by 4(1 H )-Quinolone-3-Diarylethers and Antimycin in Toxoplasma gondii

Genetic Evidence for Cytochrome b Q _i Site Inhibition by 4(1 H )-Quinolone-3-Diarylethers and Antimycin in Toxoplasma gondii