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Remodeling of ER-exit sites initiates a membrane supply pathway for autophagosome biogenesis

Liang Ge, Min Zhang, Samuel J Kenny, Dawei Liu, Miharu Maeda, Kota Saito, Anandita Mathur, Ke Xu, View ORCID ProfileRandy Schekman
doi: https://doi.org/10.1101/168518
Liang Ge
1Howard Hughes Medical Institute, and Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720;
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  • For correspondence: lge19830626@gmail.com schekman@berkeley.edu
Min Zhang
1Howard Hughes Medical Institute, and Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720;
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Samuel J Kenny
2Department of Chemistry, University of California, Berkeley, CA 94720
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Dawei Liu
1Howard Hughes Medical Institute, and Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720;
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Miharu Maeda
3Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo 113-0033, Japan
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Kota Saito
3Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo 113-0033, Japan
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Anandita Mathur
1Howard Hughes Medical Institute, and Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720;
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Ke Xu
2Department of Chemistry, University of California, Berkeley, CA 94720
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Randy Schekman
1Howard Hughes Medical Institute, and Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720;
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  • ORCID record for Randy Schekman
  • For correspondence: lge19830626@gmail.com schekman@berkeley.edu
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Abstract

Autophagosomes are double-membrane vesicles generated during autophagy. Biogenesis of the autophagosome requires membrane acquisition from intracellular compartments, the mechanisms of which are unclear. We previously found that a relocation of COPII machinery to the ER-Golgi intermediate compartment (ERGIC) generates ERGIC-derived COPII vesicles which serve as a membrane precursor for the lipidation of LC3, a key membrane component of the autophagosome. Here we employed super-resolution microscopy to show that starvation induces the enlargement of ER-exit sites (ERES) positive for the COPII activator, SEC12, and the remodeled ERES patches along the ERGIC. A SEC12 binding protein, CTAGE5, is required for the enlargement of ERES, SEC12 relocation to the ERGIC, and modulates autophagosome biogenesis. Moreover, FIP200, a subunit of the ULK protein kinase complex, facilitates the starvation-induced enlargement of ERES independent of the other subunits of this complex and associates via its C-terminal domain with SEC12. Our data indicate a pathway wherein FIP200 and CTAGE5 facilitate starvation-induced remodeling of the ERES, a prerequisite for the production of COPII vesicles budded from the ERGIC that contribute to autophagosome formation.

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Posted July 25, 2017.
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Remodeling of ER-exit sites initiates a membrane supply pathway for autophagosome biogenesis
Liang Ge, Min Zhang, Samuel J Kenny, Dawei Liu, Miharu Maeda, Kota Saito, Anandita Mathur, Ke Xu, Randy Schekman
bioRxiv 168518; doi: https://doi.org/10.1101/168518
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Remodeling of ER-exit sites initiates a membrane supply pathway for autophagosome biogenesis
Liang Ge, Min Zhang, Samuel J Kenny, Dawei Liu, Miharu Maeda, Kota Saito, Anandita Mathur, Ke Xu, Randy Schekman
bioRxiv 168518; doi: https://doi.org/10.1101/168518

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