Autophagy variation within a cell population determines cell fate through selective degradation of Fap-1

Gump, Jacob M.; Staskiewicz, Leah; Morgan, Michael J.; Bamberg, Alison; Riches, David W. H.; Thorburn, Andrew

doi:10.1038/ncb2886

Cited by 230Autophagy in Disease and TherapyCell death mechanisms and regulationUbiquitin and proteasome pathways

Autophagy variation within a cell population determines cell fate through selective degradation of Fap-1

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Gump, Jacob M., Staskiewicz, Leah, Morgan, Michael J., Bamberg, Alison, Riches, David W. H., Thorburn, Andrew·2014·Nature Cell Biology

DOI 10.1038/ncb2886PMC PMC3876036

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Abstract

Autophagy regulates cell death both positively and negatively, but the molecular basis for this paradox remains inadequately characterized. We demonstrate here that transient cell-to-cell variations in autophagy can promote either cell death or survival depending on the stimulus and cell type. By separating cells with high and low basal autophagy using flow cytometry, we demonstrate that autophagy determines which cells live or die in response to death receptor activation. We have determined that selective autophagic degradation of the phosphatase Fap-1 promotes Fas apoptosis in Type I cells, which do not require mitochondrial permeabilization for efficient apoptosis. Conversely, autophagy inhibits apoptosis in Type II cells (which require mitochondrial involvement) or on treatment with TRAIL in either Type I or II cells. These data illustrate that differences in autophagy in a cell population determine cell fate in a stimulus- and cell-type-specific manner. This example of selective autophagy of an apoptosis regulator may represent a general mechanism for context-specific regulation of cell fate by autophagy.

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FAS-driven extrinsic apoptosis is enhanced by autophagic degradation of PTPN13/FAP1.
“FAS-driven extrinsic apoptosis, which is enhanced by the autophagic degradation of protein tyrosine phosphatase, non-receptor type 13 (PTPN13; best known as FAP1) [822]”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [822]

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Autophagy variation within a cell population determines cell fate through selective degradation of Fap-1. Nat Cell Biol 16
Gump, J. M., Staskiewicz, L., Morgan, M. J., Bamberg, A., H, D. W., & Thorburn, A. (2014)
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Authors: Gump, J. M., Staskiewicz, L., Morgan, M. J., Bamberg, A., Riches, D. W. H., & Thorburn, A.
Affiliations: University of Colorado Anschutz (US)
National Jewish Health (US)
Corresponding author: Thorburn, Andrew
ORCID: Riches, David W. H.
Thorburn, Andrew
Venue: Nature Cell Biology
Publisher: Springer Science and Business Media LLC
Published: 2013-12-08
Volume: 16
Issue: 1
Pages: 47-54
ISSN: 1465-7392 (ISSN-L)
1476-4679
DOI: 10.1038/ncb2886
PMC: PMC3876036
OpenAlex: W2081826742
Cited by: 230
References: 52
Citations by year: 2026: 8 · 2025: 13 · 2024: 15 · 2023: 8 · 2022: 34 · 2021: 14 · 2020: 16 · 2019: 17 · 2018: 15 · 2017: 28 · 2016: 22 · 2015: 18 · 2014: 20 · 2013: 1
FWCI: 14.84
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Cell Biology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Cancer Center, University of Colorado
Anschutz Medical Campus, University of Colorado
National Heart, Lung, and Blood Institute (R01HL114754, R01HL068628, HL-68628)
National Cancer Institute (CA 150925, 5T32CA82086-10, T32CA082086, P30 CA46934, R01CA150925, R01CA111421, P30CA046934)
Topics: Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
Keywords: autophagy, FAP-1, selective autophagy, cell fate, apoptosis, Fas, death receptor signaling, TRAIL, mitochondrial membrane permeabilization, cellular heterogeneity
MeSH terms: Sequestosome-1 Protein, Autophagy, Cell Survival, Chloroquine, Culture Media, HeLa Cells, Humans, Models, Biological, Protein Binding, Recombinant Fusion Proteins, Apoptosis, fas Receptor, Cell Lineage, Jurkat Cells, Adaptor Proteins, Signal Transducing, Cell Proliferation, Green Fluorescent Proteins, Fas Ligand Protein, Protein Tyrosine Phosphatase, Non-Receptor Type 13, Proteolysis

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Autophagy variation within a cell population determines cell fate through selective degradation of Fap-1

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