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Depletion of a Toxoplasma porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum
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...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Company of Biologists Ltd
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8572010/ https://www.ncbi.nlm.nih.gov/pubmed/34523684 http://dx.doi.org/10.1242/jcs.255299 |
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author | Mallo, Natalia Ovciarikova, Jana Martins-Duarte, Erica S. Baehr, Stephan C. Biddau, Marco Wilde, Mary-Louise Uboldi, Alessandro D. Lemgruber, Leandro Tonkin, Christopher J. Wideman, Jeremy G. Harding, Clare R. Sheiner, Lilach |
author_facet | Mallo, Natalia Ovciarikova, Jana Martins-Duarte, Erica S. Baehr, Stephan C. Biddau, Marco Wilde, Mary-Louise Uboldi, Alessandro D. Lemgruber, Leandro Tonkin, Christopher J. Wideman, Jeremy G. Harding, Clare R. Sheiner, Lilach |
author_sort | Mallo, Natalia |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8572010 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | The Company of Biologists Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-85720102021-11-12 Depletion of a Toxoplasma porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum Mallo, Natalia Ovciarikova, Jana Martins-Duarte, Erica S. Baehr, Stephan C. Biddau, Marco Wilde, Mary-Louise Uboldi, Alessandro D. Lemgruber, Leandro Tonkin, Christopher J. Wideman, Jeremy G. Harding, Clare R. Sheiner, Lilach J Cell Sci Research Article 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. The Company of Biologists Ltd 2021-10-20 /pmc/articles/PMC8572010/ /pubmed/34523684 http://dx.doi.org/10.1242/jcs.255299 Text en © 2021. Published by The Company of Biologists Ltd https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. |
spellingShingle | Research Article Mallo, Natalia Ovciarikova, Jana Martins-Duarte, Erica S. Baehr, Stephan C. Biddau, Marco Wilde, Mary-Louise Uboldi, Alessandro D. Lemgruber, Leandro Tonkin, Christopher J. Wideman, Jeremy G. Harding, Clare R. Sheiner, Lilach Depletion of a Toxoplasma porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum |
title | Depletion of a Toxoplasma porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum |
title_full | Depletion of a Toxoplasma porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum |
title_fullStr | Depletion of a Toxoplasma porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum |
title_full_unstemmed | Depletion of a Toxoplasma porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum |
title_short | Depletion of a Toxoplasma porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum |
title_sort | depletion of a toxoplasma porin leads to defects in mitochondrial morphology and contacts with the endoplasmic reticulum |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8572010/ https://www.ncbi.nlm.nih.gov/pubmed/34523684 http://dx.doi.org/10.1242/jcs.255299 |
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