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Selective regulation of autophagy by the Iml1-Npr2-Npr3 complex in the absence of nitrogen starvation
Autophagy is an evolutionarily conserved pathway for the degradation of intracellular contents. How autophagy is regulated, especially upon changes in metabolic and nutritional state, remains poorly understood. By using a prototrophic strain of Saccharomyces cerevisiae, we observed that, unexpectedl...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Cell Biology
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3204073/ https://www.ncbi.nlm.nih.gov/pubmed/21900499 http://dx.doi.org/10.1091/mbc.E11-06-0525 |
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author | Wu, Xi Tu, Benjamin P. |
author_facet | Wu, Xi Tu, Benjamin P. |
author_sort | Wu, Xi |
collection | PubMed |
description | Autophagy is an evolutionarily conserved pathway for the degradation of intracellular contents. How autophagy is regulated, especially upon changes in metabolic and nutritional state, remains poorly understood. By using a prototrophic strain of Saccharomyces cerevisiae, we observed that, unexpectedly, autophagy is strongly induced simply upon switch from a rich medium to a minimal medium in the complete absence of nitrogen starvation. This novel form of autophagy was termed “non-nitrogen-starvation (NNS)–induced autophagy.” A visual screen uncovered three regulators of autophagy—Iml1p, Npr2p, and Npr3p—which function in the same complex and are selectively required for NNS-induced autophagy. During NNS-induced autophagy, Iml1p localized to either preautophagosomal structures (PAS) or non-PAS punctate structures. This localization suggests that Iml1p or the Iml1p-Npr2p-Npr3p complex might regulate autophagosome formation. Ultrastructural analysis confirmed that autophagosome formation was strongly impaired in Δiml1, Δnpr2, and Δnpr3 cells during NNS-induced autophagy. Moreover, Iml1p contains a conserved domain that is required for NNS-induced autophagy as well as complex formation. Collectively, our findings have revealed the existence of additional mechanisms that regulate autophagy under previously unrecognized conditions, in response to relatively more subtle changes in metabolic and nutritional state. |
format | Online Article Text |
id | pubmed-3204073 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | The American Society for Cell Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-32040732012-01-16 Selective regulation of autophagy by the Iml1-Npr2-Npr3 complex in the absence of nitrogen starvation Wu, Xi Tu, Benjamin P. Mol Biol Cell Articles Autophagy is an evolutionarily conserved pathway for the degradation of intracellular contents. How autophagy is regulated, especially upon changes in metabolic and nutritional state, remains poorly understood. By using a prototrophic strain of Saccharomyces cerevisiae, we observed that, unexpectedly, autophagy is strongly induced simply upon switch from a rich medium to a minimal medium in the complete absence of nitrogen starvation. This novel form of autophagy was termed “non-nitrogen-starvation (NNS)–induced autophagy.” A visual screen uncovered three regulators of autophagy—Iml1p, Npr2p, and Npr3p—which function in the same complex and are selectively required for NNS-induced autophagy. During NNS-induced autophagy, Iml1p localized to either preautophagosomal structures (PAS) or non-PAS punctate structures. This localization suggests that Iml1p or the Iml1p-Npr2p-Npr3p complex might regulate autophagosome formation. Ultrastructural analysis confirmed that autophagosome formation was strongly impaired in Δiml1, Δnpr2, and Δnpr3 cells during NNS-induced autophagy. Moreover, Iml1p contains a conserved domain that is required for NNS-induced autophagy as well as complex formation. Collectively, our findings have revealed the existence of additional mechanisms that regulate autophagy under previously unrecognized conditions, in response to relatively more subtle changes in metabolic and nutritional state. The American Society for Cell Biology 2011-11-01 /pmc/articles/PMC3204073/ /pubmed/21900499 http://dx.doi.org/10.1091/mbc.E11-06-0525 Text en © 2011 Wu and Tu. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society of Cell Biology. |
spellingShingle | Articles Wu, Xi Tu, Benjamin P. Selective regulation of autophagy by the Iml1-Npr2-Npr3 complex in the absence of nitrogen starvation |
title | Selective regulation of autophagy by the Iml1-Npr2-Npr3 complex in the absence of nitrogen starvation |
title_full | Selective regulation of autophagy by the Iml1-Npr2-Npr3 complex in the absence of nitrogen starvation |
title_fullStr | Selective regulation of autophagy by the Iml1-Npr2-Npr3 complex in the absence of nitrogen starvation |
title_full_unstemmed | Selective regulation of autophagy by the Iml1-Npr2-Npr3 complex in the absence of nitrogen starvation |
title_short | Selective regulation of autophagy by the Iml1-Npr2-Npr3 complex in the absence of nitrogen starvation |
title_sort | selective regulation of autophagy by the iml1-npr2-npr3 complex in the absence of nitrogen starvation |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3204073/ https://www.ncbi.nlm.nih.gov/pubmed/21900499 http://dx.doi.org/10.1091/mbc.E11-06-0525 |
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