Phosphatidylinositol 3-kinase and COPII generate LC3 lipidation vesicles from the ER-Golgi intermediate compartment
Formation of the autophagosome requires significant membrane input from cellular organelles. However, no direct evidence has been developed to link autophagic factors and the mobilization of membranes to generate the phagophore. Previously, we established a cell-free LC3 lipidation reaction to ident...
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doaj-7636b0495d384d66a9019641c390fae92021-05-04T23:33:27ZengeLife Sciences Publications LtdeLife2050-084X2014-11-01310.7554/eLife.04135Phosphatidylinositol 3-kinase and COPII generate LC3 lipidation vesicles from the ER-Golgi intermediate compartmentLiang Ge0Min Zhang1Randy Schekman2Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, United StatesDepartment of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, United StatesDepartment of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, United StatesFormation of the autophagosome requires significant membrane input from cellular organelles. However, no direct evidence has been developed to link autophagic factors and the mobilization of membranes to generate the phagophore. Previously, we established a cell-free LC3 lipidation reaction to identify the ER-Golgi intermediate compartment (ERGIC) as a membrane source for LC3 lipidation, a key step of autophagosome biogenesis (Ge et al., eLife 2013; 2:e00947). We now report that starvation activation of autophagic phosphotidylinositol-3 kinase (PI3K) induces the generation of small vesicles active in LC3 lipidation. Subcellular fractionation studies identified the ERGIC as the donor membrane in the generation of small lipidation-active vesicles. COPII proteins are recruited to the ERGIC membrane in starved cells, dependent on active PI3K. We conclude that starvation activates the autophagic PI3K, which in turn induces the recruitment of COPII to the ERGIC to bud LC3 lipidation-active vesicles as one potential membrane source of the autophagosome.https://elifesciences.org/articles/04135autophagyautophagosomeCOPIIER-Golgi intermediate compartmentLC3 lipidationPhosphatidylinositol 3-kinase |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Liang Ge Min Zhang Randy Schekman |
spellingShingle |
Liang Ge Min Zhang Randy Schekman Phosphatidylinositol 3-kinase and COPII generate LC3 lipidation vesicles from the ER-Golgi intermediate compartment eLife autophagy autophagosome COPII ER-Golgi intermediate compartment LC3 lipidation Phosphatidylinositol 3-kinase |
author_facet |
Liang Ge Min Zhang Randy Schekman |
author_sort |
Liang Ge |
title |
Phosphatidylinositol 3-kinase and COPII generate LC3 lipidation vesicles from the ER-Golgi intermediate compartment |
title_short |
Phosphatidylinositol 3-kinase and COPII generate LC3 lipidation vesicles from the ER-Golgi intermediate compartment |
title_full |
Phosphatidylinositol 3-kinase and COPII generate LC3 lipidation vesicles from the ER-Golgi intermediate compartment |
title_fullStr |
Phosphatidylinositol 3-kinase and COPII generate LC3 lipidation vesicles from the ER-Golgi intermediate compartment |
title_full_unstemmed |
Phosphatidylinositol 3-kinase and COPII generate LC3 lipidation vesicles from the ER-Golgi intermediate compartment |
title_sort |
phosphatidylinositol 3-kinase and copii generate lc3 lipidation vesicles from the er-golgi intermediate compartment |
publisher |
eLife Sciences Publications Ltd |
series |
eLife |
issn |
2050-084X |
publishDate |
2014-11-01 |
description |
Formation of the autophagosome requires significant membrane input from cellular organelles. However, no direct evidence has been developed to link autophagic factors and the mobilization of membranes to generate the phagophore. Previously, we established a cell-free LC3 lipidation reaction to identify the ER-Golgi intermediate compartment (ERGIC) as a membrane source for LC3 lipidation, a key step of autophagosome biogenesis (Ge et al., eLife 2013; 2:e00947). We now report that starvation activation of autophagic phosphotidylinositol-3 kinase (PI3K) induces the generation of small vesicles active in LC3 lipidation. Subcellular fractionation studies identified the ERGIC as the donor membrane in the generation of small lipidation-active vesicles. COPII proteins are recruited to the ERGIC membrane in starved cells, dependent on active PI3K. We conclude that starvation activates the autophagic PI3K, which in turn induces the recruitment of COPII to the ERGIC to bud LC3 lipidation-active vesicles as one potential membrane source of the autophagosome. |
topic |
autophagy autophagosome COPII ER-Golgi intermediate compartment LC3 lipidation Phosphatidylinositol 3-kinase |
url |
https://elifesciences.org/articles/04135 |
work_keys_str_mv |
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1721476982541123584 |