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Drosophila Porin/VDAC Affects Mitochondrial Morphology

Voltage-dependent anion channel (VDAC) has been suggested to be a mediator of mitochondrial-dependent cell death induced by Ca(2+) overload, oxidative stress and Bax-Bid activation. To confirm this hypothesis in vivo, we generated and characterized Drosophila VDAC (porin) mutants and found that Pori...

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Autores principales: Park, Jeehye, Kim, Yongsung, Choi, Sekyu, Koh, Hyongjong, Lee, Sang-Hee, Kim, Jin-Man, Chung, Jongkyeong
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2951900/
https://www.ncbi.nlm.nih.gov/pubmed/20949033
http://dx.doi.org/10.1371/journal.pone.0013151
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author Park, Jeehye
Kim, Yongsung
Choi, Sekyu
Koh, Hyongjong
Lee, Sang-Hee
Kim, Jin-Man
Chung, Jongkyeong
author_facet Park, Jeehye
Kim, Yongsung
Choi, Sekyu
Koh, Hyongjong
Lee, Sang-Hee
Kim, Jin-Man
Chung, Jongkyeong
author_sort Park, Jeehye
collection PubMed
description Voltage-dependent anion channel (VDAC) has been suggested to be a mediator of mitochondrial-dependent cell death induced by Ca(2+) overload, oxidative stress and Bax-Bid activation. To confirm this hypothesis in vivo, we generated and characterized Drosophila VDAC (porin) mutants and found that Porin is not required for mitochondrial apoptosis, which is consistent with the previous mouse studies. We also reported a novel physiological role of Porin. Loss of porin resulted in locomotive defects and male sterility. Intriguingly, porin mutants exhibited elongated mitochondria in indirect flight muscle, whereas Porin overexpression produced fragmented mitochondria. Through genetic analysis with the components of mitochondrial fission and fusion, we found that the elongated mitochondria phenotype in porin mutants were suppressed by increased mitochondrial fission, but enhanced by increased mitochondrial fusion. Furthermore, increased mitochondrial fission by Drp1 expression suppressed the flight defects in the porin mutants. Collectively, our study showed that loss of Drosophila Porin results in mitochondrial morphological defects and suggested that the defective mitochondrial function by Porin deficiency affects the mitochondrial remodeling process.
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spelling pubmed-29519002010-10-14 Drosophila Porin/VDAC Affects Mitochondrial Morphology Park, Jeehye Kim, Yongsung Choi, Sekyu Koh, Hyongjong Lee, Sang-Hee Kim, Jin-Man Chung, Jongkyeong PLoS One Research Article Voltage-dependent anion channel (VDAC) has been suggested to be a mediator of mitochondrial-dependent cell death induced by Ca(2+) overload, oxidative stress and Bax-Bid activation. To confirm this hypothesis in vivo, we generated and characterized Drosophila VDAC (porin) mutants and found that Porin is not required for mitochondrial apoptosis, which is consistent with the previous mouse studies. We also reported a novel physiological role of Porin. Loss of porin resulted in locomotive defects and male sterility. Intriguingly, porin mutants exhibited elongated mitochondria in indirect flight muscle, whereas Porin overexpression produced fragmented mitochondria. Through genetic analysis with the components of mitochondrial fission and fusion, we found that the elongated mitochondria phenotype in porin mutants were suppressed by increased mitochondrial fission, but enhanced by increased mitochondrial fusion. Furthermore, increased mitochondrial fission by Drp1 expression suppressed the flight defects in the porin mutants. Collectively, our study showed that loss of Drosophila Porin results in mitochondrial morphological defects and suggested that the defective mitochondrial function by Porin deficiency affects the mitochondrial remodeling process. Public Library of Science 2010-10-07 /pmc/articles/PMC2951900/ /pubmed/20949033 http://dx.doi.org/10.1371/journal.pone.0013151 Text en Park et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Park, Jeehye
Kim, Yongsung
Choi, Sekyu
Koh, Hyongjong
Lee, Sang-Hee
Kim, Jin-Man
Chung, Jongkyeong
Drosophila Porin/VDAC Affects Mitochondrial Morphology
title Drosophila Porin/VDAC Affects Mitochondrial Morphology
title_full Drosophila Porin/VDAC Affects Mitochondrial Morphology
title_fullStr Drosophila Porin/VDAC Affects Mitochondrial Morphology
title_full_unstemmed Drosophila Porin/VDAC Affects Mitochondrial Morphology
title_short Drosophila Porin/VDAC Affects Mitochondrial Morphology
title_sort drosophila porin/vdac affects mitochondrial morphology
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2951900/
https://www.ncbi.nlm.nih.gov/pubmed/20949033
http://dx.doi.org/10.1371/journal.pone.0013151
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