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Nature Cell Biology
Article
License: implied-oa
Data sources: UnpayWall
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PubMed Central
Other literature type . 2013
Data sources: PubMed Central
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Nature Cell Biology
Article . 2013 . Peer-reviewed
License: Springer TDM
Data sources: Crossref
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Uba1 functions in Atg7- and Atg3-independent autophagy

Authors: Chang, Tsun-Kai; Shravage, Bhupendra V.; Hayes, Sebastian D.; Powers, Christine M.; Simin, Rachel T.; Wade Harper, J.; Baehrecke, Eric H.;

Uba1 functions in Atg7- and Atg3-independent autophagy

Abstract

Autophagy is a conserved process that delivers components of the cytoplasm to lysosomes for degradation. The E1 and E2 enzymes encoded by Atg7 and Atg3 are thought to be essential for autophagy involving the ubiquitin-like protein Atg8. Here, we describe an Atg7- and Atg3-independent autophagy pathway that facilitates programmed reduction of cell size during intestine cell death. Although multiple components of the core autophagy pathways, including Atg8, are required for autophagy and cells to shrink in the midgut of the intestine, loss of either Atg7 or Atg3 function does not influence these cellular processes. Rather, Uba1, the E1 enzyme used in ubiquitylation, is required for autophagy and reduction of cell size. Our data reveal that distinct autophagy programs are used by different cells within an animal, and disclose an unappreciated role for ubiquitin activation in autophagy.

Keywords

Investigative Techniques, 570, Cells, 610, Ubiquitin-Activating Enzymes, Autophagy-Related Protein 7, Article, Enzymes and Coenzymes, Autophagy, Animals, Drosophila Proteins, Protein Isoforms, Amino Acids, Cell Size, Ubiquitin, and Proteins, Ubiquitination, Epithelial Cells, Cell Biology, Cellular and Molecular Physiology, Intestines, Drosophila melanogaster, Gene Expression Regulation, Organ Specificity, Larva, Ubiquitin-Conjugating Enzymes, Peptides, Signal Transduction

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    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    168
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 1%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 1%
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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
168
Top 1%
Top 10%
Top 1%
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hybrid