Depletion of a <i>Toxoplasma</i> porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum
Natalia Mallo, Jana Ovciarikova, Érica S. Martins-Duarte, Stephan Baehr, Marco Biddau, Mary‐Louise Wilde, Alessandro D. Uboldi, Leandro Lemgruber, Christopher J. Tonkin, Jeremy G. Wideman, Clare R. Harding, Lilach Sheiner
Abstract
The voltage-dependent anion channel (VDAC) is a ubiquitous channel in the outer membrane of the mitochondrion with multiple roles in protein, metabolite and small molecule transport. In mammalian cells, VDAC protein, as part of a larger complex including the inositol triphosphate receptor, has been shown to have a role in mediating contacts between the mitochondria and endoplasmic reticulum (ER). We identify VDAC of the pathogenic apicomplexan Toxoplasma gondii and demonstrate its importance for parasite growth. We show that VDAC is involved in protein import and metabolite transfer to mitochondria. Further, depletion of VDAC resulted in significant morphological changes in the mitochondrion and ER, suggesting a role in mediating contacts between these organelles in T. gondii. This article has an associated First Person interview with the first author of the paper.