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TORC1 inactivation stimulates autophagy of nucleoporin and nuclear pore complexes

The mechanisms underlying turnover of the nuclear pore complex (NPC) and the component nucleoporins (Nups) are still poorly understood. In this study, we found that the budding yeast Saccharomyces cerevisiae triggers NPC degradation by autophagy upon the inactivation of Tor kinase complex 1. This de...

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Autores principales: Tomioka, Yui, Kotani, Tetsuya, Kirisako, Hiromi, Oikawa, Yu, Kimura, Yayoi, Hirano, Hisashi, Ohsumi, Yoshinori, Nakatogawa, Hitoshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Rockefeller University Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7337488/
https://www.ncbi.nlm.nih.gov/pubmed/32453403
http://dx.doi.org/10.1083/jcb.201910063
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author Tomioka, Yui
Kotani, Tetsuya
Kirisako, Hiromi
Oikawa, Yu
Kimura, Yayoi
Hirano, Hisashi
Ohsumi, Yoshinori
Nakatogawa, Hitoshi
author_facet Tomioka, Yui
Kotani, Tetsuya
Kirisako, Hiromi
Oikawa, Yu
Kimura, Yayoi
Hirano, Hisashi
Ohsumi, Yoshinori
Nakatogawa, Hitoshi
author_sort Tomioka, Yui
collection PubMed
description The mechanisms underlying turnover of the nuclear pore complex (NPC) and the component nucleoporins (Nups) are still poorly understood. In this study, we found that the budding yeast Saccharomyces cerevisiae triggers NPC degradation by autophagy upon the inactivation of Tor kinase complex 1. This degradation largely depends on the selective autophagy-specific factor Atg11 and the autophagy receptor–binding ability of Atg8, suggesting that the NPC is degraded via receptor-dependent selective autophagy. Immunoelectron microscopy revealed that NPCs embedded in nuclear envelope–derived double-membrane vesicles are sequestered within autophagosomes. At least two pathways are involved in NPC degradation: Atg39-dependent nucleophagy (selective autophagy of the nucleus) and a pathway involving an unknown receptor. In addition, we found the interaction between Nup159 and Atg8 via the Atg8-family interacting motif is important for degradation of this nucleoporin not assembled into the NPC. Thus, this study provides the first evidence for autophagic degradation of the NPC and Nups, which we term “NPC-phagy” and “nucleoporinophagy.”
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spelling pubmed-73374882021-01-06 TORC1 inactivation stimulates autophagy of nucleoporin and nuclear pore complexes Tomioka, Yui Kotani, Tetsuya Kirisako, Hiromi Oikawa, Yu Kimura, Yayoi Hirano, Hisashi Ohsumi, Yoshinori Nakatogawa, Hitoshi J Cell Biol Report The mechanisms underlying turnover of the nuclear pore complex (NPC) and the component nucleoporins (Nups) are still poorly understood. In this study, we found that the budding yeast Saccharomyces cerevisiae triggers NPC degradation by autophagy upon the inactivation of Tor kinase complex 1. This degradation largely depends on the selective autophagy-specific factor Atg11 and the autophagy receptor–binding ability of Atg8, suggesting that the NPC is degraded via receptor-dependent selective autophagy. Immunoelectron microscopy revealed that NPCs embedded in nuclear envelope–derived double-membrane vesicles are sequestered within autophagosomes. At least two pathways are involved in NPC degradation: Atg39-dependent nucleophagy (selective autophagy of the nucleus) and a pathway involving an unknown receptor. In addition, we found the interaction between Nup159 and Atg8 via the Atg8-family interacting motif is important for degradation of this nucleoporin not assembled into the NPC. Thus, this study provides the first evidence for autophagic degradation of the NPC and Nups, which we term “NPC-phagy” and “nucleoporinophagy.” Rockefeller University Press 2020-05-26 /pmc/articles/PMC7337488/ /pubmed/32453403 http://dx.doi.org/10.1083/jcb.201910063 Text en © 2020 Tomioka et al. http://www.rupress.org/terms/https://creativecommons.org/licenses/by-nc-sa/4.0/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Report
Tomioka, Yui
Kotani, Tetsuya
Kirisako, Hiromi
Oikawa, Yu
Kimura, Yayoi
Hirano, Hisashi
Ohsumi, Yoshinori
Nakatogawa, Hitoshi
TORC1 inactivation stimulates autophagy of nucleoporin and nuclear pore complexes
title TORC1 inactivation stimulates autophagy of nucleoporin and nuclear pore complexes
title_full TORC1 inactivation stimulates autophagy of nucleoporin and nuclear pore complexes
title_fullStr TORC1 inactivation stimulates autophagy of nucleoporin and nuclear pore complexes
title_full_unstemmed TORC1 inactivation stimulates autophagy of nucleoporin and nuclear pore complexes
title_short TORC1 inactivation stimulates autophagy of nucleoporin and nuclear pore complexes
title_sort torc1 inactivation stimulates autophagy of nucleoporin and nuclear pore complexes
topic Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7337488/
https://www.ncbi.nlm.nih.gov/pubmed/32453403
http://dx.doi.org/10.1083/jcb.201910063
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