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Atlastins mediate selective autophagy of the endoplasmic reticulum

Jin Rui Liang, Emily Lingeman, Saba Ahmed, Jacob Corn
doi: https://doi.org/10.1101/274530
Jin Rui Liang
1Innovative Genomics Institute, University of California, Berkeley, CA 94720
2Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720
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Emily Lingeman
1Innovative Genomics Institute, University of California, Berkeley, CA 94720
2Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720
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Saba Ahmed
1Innovative Genomics Institute, University of California, Berkeley, CA 94720
2Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720
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Jacob Corn
1Innovative Genomics Institute, University of California, Berkeley, CA 94720
2Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720
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  • For correspondence: jcorn@berkeley.edu
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ABSTRACT

The selective lysosomal degradation (autophagy) of entire organelles is required for cellular homeostasis, and its dysregulation is involved in degenerative disorders such as Parkinson’s Disease. While autophagy of mitochondria (mitophagy) is becoming better understood, other forms of organelle autophagy are relatively unexplored. Here we develope multiple quantitative assays to measure organelle autophagy using flow cytometry, microscopy, and Western blotting. Focusing on autophagy of the endoplasmic reticulum (ER-phagy), we show that these assays allow facile measurement of ER-phagy, and that ER-phagy is inhibited by knockdown of either core autophagy components or the recently reported FAM134B ER-phagy receptor. Using these assays, we further identify that Atlastins, the ER-resident GTPases involved in ER membrane morphology, are key positive effectors of ER-phagy. Atlastin-depleted cells have decreased ER-phagy under starvation conditions, and Atlastin’s role in ER-phagy requires both a functional GTPase domain and proper ER localization. The three Atlastin family members functionally compensate for one another during ER-phagy and may form heteromeric complexes with one another. We also find that Atlastins act downstream of the FAM134B ER-phagy receptor. We propose that during ER-phagy, Atlastins remodel ER membrane to separate pieces of FAM134B-marked ER for efficient autophagosomal engulfment. Human mutations in Atlastins led to hereditary spastic paraplegia, and our results suggest that this disease may be linked to deficiencies in ER-phagy rather than ER morphology.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted March 01, 2018.
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Atlastins mediate selective autophagy of the endoplasmic reticulum
Jin Rui Liang, Emily Lingeman, Saba Ahmed, Jacob Corn
bioRxiv 274530; doi: https://doi.org/10.1101/274530
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Atlastins mediate selective autophagy of the endoplasmic reticulum
Jin Rui Liang, Emily Lingeman, Saba Ahmed, Jacob Corn
bioRxiv 274530; doi: https://doi.org/10.1101/274530

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