Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice
Autophagy is a membrane-trafficking mechanism that delivers cytoplasmic constituents into the lysosome/vacuole for bulk protein degradation. This mechanism is involved in the preservation of nutrients under starvation condition as well as the normal turnover of cytoplasmic component. Aberrant autoph...
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2005
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pubmed-21719282008-03-05 Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice Komatsu, Masaaki Waguri, Satoshi Ueno, Takashi Iwata, Junichi Murata, Shigeo Tanida, Isei Ezaki, Junji Mizushima, Noboru Ohsumi, Yoshinori Uchiyama, Yasuo Kominami, Eiki Tanaka, Keiji Chiba, Tomoki Research Articles Autophagy is a membrane-trafficking mechanism that delivers cytoplasmic constituents into the lysosome/vacuole for bulk protein degradation. This mechanism is involved in the preservation of nutrients under starvation condition as well as the normal turnover of cytoplasmic component. Aberrant autophagy has been reported in several neurodegenerative disorders, hepatitis, and myopathies. Here, we generated conditional knockout mice of Atg7, an essential gene for autophagy in yeast. Atg7 was essential for ATG conjugation systems and autophagosome formation, amino acid supply in neonates, and starvation-induced bulk degradation of proteins and organelles in mice. Furthermore, Atg7 deficiency led to multiple cellular abnormalities, such as appearance of concentric membranous structure and deformed mitochondria, and accumulation of ubiquitin-positive aggregates. Our results indicate the important role of autophagy in starvation response and the quality control of proteins and organelles in quiescent cells. The Rockefeller University Press 2005-05-09 /pmc/articles/PMC2171928/ /pubmed/15866887 http://dx.doi.org/10.1083/jcb.200412022 Text en Copyright © 2005, The Rockefeller University Press 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 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
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Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Komatsu, Masaaki Waguri, Satoshi Ueno, Takashi Iwata, Junichi Murata, Shigeo Tanida, Isei Ezaki, Junji Mizushima, Noboru Ohsumi, Yoshinori Uchiyama, Yasuo Kominami, Eiki Tanaka, Keiji Chiba, Tomoki |
spellingShingle |
Komatsu, Masaaki Waguri, Satoshi Ueno, Takashi Iwata, Junichi Murata, Shigeo Tanida, Isei Ezaki, Junji Mizushima, Noboru Ohsumi, Yoshinori Uchiyama, Yasuo Kominami, Eiki Tanaka, Keiji Chiba, Tomoki Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice |
author_facet |
Komatsu, Masaaki Waguri, Satoshi Ueno, Takashi Iwata, Junichi Murata, Shigeo Tanida, Isei Ezaki, Junji Mizushima, Noboru Ohsumi, Yoshinori Uchiyama, Yasuo Kominami, Eiki Tanaka, Keiji Chiba, Tomoki |
author_sort |
Komatsu, Masaaki |
title |
Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice |
title_short |
Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice |
title_full |
Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice |
title_fullStr |
Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice |
title_full_unstemmed |
Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice |
title_sort |
impairment of starvation-induced and constitutive autophagy in atg7-deficient mice |
description |
Autophagy is a membrane-trafficking mechanism that delivers cytoplasmic constituents into the lysosome/vacuole for bulk protein degradation. This mechanism is involved in the preservation of nutrients under starvation condition as well as the normal turnover of cytoplasmic component. Aberrant autophagy has been reported in several neurodegenerative disorders, hepatitis, and myopathies. Here, we generated conditional knockout mice of Atg7, an essential gene for autophagy in yeast. Atg7 was essential for ATG conjugation systems and autophagosome formation, amino acid supply in neonates, and starvation-induced bulk degradation of proteins and organelles in mice. Furthermore, Atg7 deficiency led to multiple cellular abnormalities, such as appearance of concentric membranous structure and deformed mitochondria, and accumulation of ubiquitin-positive aggregates. Our results indicate the important role of autophagy in starvation response and the quality control of proteins and organelles in quiescent cells. |
publisher |
The Rockefeller University Press |
publishDate |
2005 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2171928/ |
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1611424752599040000 |