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Sec20 Is Required for Autophagic and Endocytic Degradation Independent of Golgi-ER Retrograde Transport
Endocytosis and autophagy are evolutionarily conserved degradative processes in all eukaryotes. Both pathways converge to the lysosome where cargo is degraded. Improper lysosomal degradation is observed in many human pathologies, so its regulatory mechanisms are important to understand. Sec20/BNIP1...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6721519/ https://www.ncbi.nlm.nih.gov/pubmed/31344970 http://dx.doi.org/10.3390/cells8080768 |
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author | Lakatos, Zsolt Lőrincz, Péter Szabó, Zoltán Benkő, Péter Kenéz, Lili Anna Csizmadia, Tamás Juhász, Gábor |
author_facet | Lakatos, Zsolt Lőrincz, Péter Szabó, Zoltán Benkő, Péter Kenéz, Lili Anna Csizmadia, Tamás Juhász, Gábor |
author_sort | Lakatos, Zsolt |
collection | PubMed |
description | Endocytosis and autophagy are evolutionarily conserved degradative processes in all eukaryotes. Both pathways converge to the lysosome where cargo is degraded. Improper lysosomal degradation is observed in many human pathologies, so its regulatory mechanisms are important to understand. Sec20/BNIP1 (BCL2/adenovirus E1B 19 kDa protein-interacting protein 1) is a BH3 (Bcl-2 homology 3) domain-containing SNARE (soluble N-ethylmaleimide-sensitive factor-attachment protein receptors) protein that has been suggested to promote Golgi-ER retrograde transport, mitochondrial fission, apoptosis and mitophagy in yeast and vertebrates. Here, we show that loss of Sec20 in Drosophila fat cells causes the accumulation of autophagic vesicles and prevents proper lysosomal acidification and degradation during bulk, starvation-induced autophagy. Furthermore, Sec20 knockdown leads to the enlargement of late endosomes and accumulation of defective endolysosomes in larval Drosophila nephrocytes. Importantly, the loss of Syx18 (Syntaxin 18), one of the known partners of Sec20, led to similar changes in nephrocytes and fat cells. Interestingly. Sec20 appears to function independent of its role in Golgi-ER retrograde transport in regulating lysosomal degradation, as the loss of its other partner SNAREs Use1 (Unconventional SNARE In The ER 1) and Sec22 or tethering factor Zw10 (Zeste white 10), which function together in the Golgi-ER pathway, does not cause defects in autophagy or endocytosis. Thus, our data identify a potential new transport route specific to lysosome biogenesis and function. |
format | Online Article Text |
id | pubmed-6721519 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-67215192019-09-10 Sec20 Is Required for Autophagic and Endocytic Degradation Independent of Golgi-ER Retrograde Transport Lakatos, Zsolt Lőrincz, Péter Szabó, Zoltán Benkő, Péter Kenéz, Lili Anna Csizmadia, Tamás Juhász, Gábor Cells Article Endocytosis and autophagy are evolutionarily conserved degradative processes in all eukaryotes. Both pathways converge to the lysosome where cargo is degraded. Improper lysosomal degradation is observed in many human pathologies, so its regulatory mechanisms are important to understand. Sec20/BNIP1 (BCL2/adenovirus E1B 19 kDa protein-interacting protein 1) is a BH3 (Bcl-2 homology 3) domain-containing SNARE (soluble N-ethylmaleimide-sensitive factor-attachment protein receptors) protein that has been suggested to promote Golgi-ER retrograde transport, mitochondrial fission, apoptosis and mitophagy in yeast and vertebrates. Here, we show that loss of Sec20 in Drosophila fat cells causes the accumulation of autophagic vesicles and prevents proper lysosomal acidification and degradation during bulk, starvation-induced autophagy. Furthermore, Sec20 knockdown leads to the enlargement of late endosomes and accumulation of defective endolysosomes in larval Drosophila nephrocytes. Importantly, the loss of Syx18 (Syntaxin 18), one of the known partners of Sec20, led to similar changes in nephrocytes and fat cells. Interestingly. Sec20 appears to function independent of its role in Golgi-ER retrograde transport in regulating lysosomal degradation, as the loss of its other partner SNAREs Use1 (Unconventional SNARE In The ER 1) and Sec22 or tethering factor Zw10 (Zeste white 10), which function together in the Golgi-ER pathway, does not cause defects in autophagy or endocytosis. Thus, our data identify a potential new transport route specific to lysosome biogenesis and function. MDPI 2019-07-24 /pmc/articles/PMC6721519/ /pubmed/31344970 http://dx.doi.org/10.3390/cells8080768 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Lakatos, Zsolt Lőrincz, Péter Szabó, Zoltán Benkő, Péter Kenéz, Lili Anna Csizmadia, Tamás Juhász, Gábor Sec20 Is Required for Autophagic and Endocytic Degradation Independent of Golgi-ER Retrograde Transport |
title | Sec20 Is Required for Autophagic and Endocytic Degradation Independent of Golgi-ER Retrograde Transport |
title_full | Sec20 Is Required for Autophagic and Endocytic Degradation Independent of Golgi-ER Retrograde Transport |
title_fullStr | Sec20 Is Required for Autophagic and Endocytic Degradation Independent of Golgi-ER Retrograde Transport |
title_full_unstemmed | Sec20 Is Required for Autophagic and Endocytic Degradation Independent of Golgi-ER Retrograde Transport |
title_short | Sec20 Is Required for Autophagic and Endocytic Degradation Independent of Golgi-ER Retrograde Transport |
title_sort | sec20 is required for autophagic and endocytic degradation independent of golgi-er retrograde transport |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6721519/ https://www.ncbi.nlm.nih.gov/pubmed/31344970 http://dx.doi.org/10.3390/cells8080768 |
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