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Regulatory Mechanisms of Mitochondrial Autophagy: Lessons From Yeast

Mitochondria produce the majority of ATP required by cells via oxidative phosphorylation. Therefore, regulation of mitochondrial quality and quantity is important for maintaining cellular activities. Mitophagy, the selective degradation of mitochondria, is thought to contribute to control of mitocho...

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Autores principales: Furukawa, Kentaro, Innokentev, Aleksei, Kanki, Tomotake
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6872543/
https://www.ncbi.nlm.nih.gov/pubmed/31803214
http://dx.doi.org/10.3389/fpls.2019.01479
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author Furukawa, Kentaro
Innokentev, Aleksei
Kanki, Tomotake
author_facet Furukawa, Kentaro
Innokentev, Aleksei
Kanki, Tomotake
author_sort Furukawa, Kentaro
collection PubMed
description Mitochondria produce the majority of ATP required by cells via oxidative phosphorylation. Therefore, regulation of mitochondrial quality and quantity is important for maintaining cellular activities. Mitophagy, the selective degradation of mitochondria, is thought to contribute to control of mitochondrial quality and quantity. In recent years, the molecular mechanism of mitophagy has been extensively studied in yeast and mammalian cells. In particular, identification of the mitophagy receptor Atg32 has contributed to substantial progress in understanding of mitophagy in yeast. This review summarizes the molecular mechanism of mitophagy in yeast and compares it to the mechanism of mitophagy in mammals. We also discuss the current understanding of mitophagy in plants.
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spelling pubmed-68725432019-12-04 Regulatory Mechanisms of Mitochondrial Autophagy: Lessons From Yeast Furukawa, Kentaro Innokentev, Aleksei Kanki, Tomotake Front Plant Sci Plant Science Mitochondria produce the majority of ATP required by cells via oxidative phosphorylation. Therefore, regulation of mitochondrial quality and quantity is important for maintaining cellular activities. Mitophagy, the selective degradation of mitochondria, is thought to contribute to control of mitochondrial quality and quantity. In recent years, the molecular mechanism of mitophagy has been extensively studied in yeast and mammalian cells. In particular, identification of the mitophagy receptor Atg32 has contributed to substantial progress in understanding of mitophagy in yeast. This review summarizes the molecular mechanism of mitophagy in yeast and compares it to the mechanism of mitophagy in mammals. We also discuss the current understanding of mitophagy in plants. Frontiers Media S.A. 2019-11-15 /pmc/articles/PMC6872543/ /pubmed/31803214 http://dx.doi.org/10.3389/fpls.2019.01479 Text en Copyright © 2019 Furukawa, Innokentev and Kanki http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Plant Science
Furukawa, Kentaro
Innokentev, Aleksei
Kanki, Tomotake
Regulatory Mechanisms of Mitochondrial Autophagy: Lessons From Yeast
title Regulatory Mechanisms of Mitochondrial Autophagy: Lessons From Yeast
title_full Regulatory Mechanisms of Mitochondrial Autophagy: Lessons From Yeast
title_fullStr Regulatory Mechanisms of Mitochondrial Autophagy: Lessons From Yeast
title_full_unstemmed Regulatory Mechanisms of Mitochondrial Autophagy: Lessons From Yeast
title_short Regulatory Mechanisms of Mitochondrial Autophagy: Lessons From Yeast
title_sort regulatory mechanisms of mitochondrial autophagy: lessons from yeast
topic Plant Science
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6872543/
https://www.ncbi.nlm.nih.gov/pubmed/31803214
http://dx.doi.org/10.3389/fpls.2019.01479
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