Depletion of a Toxoplasma porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum
Author(s) -
Natalia Mallo,
Jana Ovciarikova,
Érica S. Martins-Duarte,
Stephan Baehr,
Marco Biddau,
MaryLouise Wilde,
Alessandro D. Uboldi,
Leandro Lemgruber,
Christopher J. Tonkin,
Jeremy G. Wideman,
Clare R. Harding,
Lilach Sheiner
Publication year - 2021
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.255299
Subject(s) - voltage dependent anion channel , endoplasmic reticulum , biology , mitochondrion , porin , microbiology and biotechnology , stim1 , organelle , bacterial outer membrane , toxoplasma gondii , vdac1 , biochemistry , immunology , escherichia coli , antibody , gene
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.
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