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Hsc70/Stub1 promotes the removal of individual oxidatively stressed peroxisomes

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  • Bo-Hua Chen

    (Taiwan International Graduate Program, Academia Sinica
    Academia Sinica
    National Tsing Hua University)

  • Yao-Jen Chang

    (Academia Sinica)

  • Steven Lin

    (Academia Sinica
    National Taiwan University)

  • Wei Yuan Yang

    (Taiwan International Graduate Program, Academia Sinica
    Academia Sinica
    National Taiwan University)

Abstract

Peroxisomes perform beta-oxidation of branched and very-long chain fatty acids, which leads to the formation of reactive oxygen species (ROS) within the peroxisomal lumen. Peroxisomes are therefore prone to ROS-mediated damages. Here, using light to specifically and acutely induce ROS formation within the peroxisomal lumen, we find that cells individually remove ROS-stressed peroxisomes through ubiquitin-dependent pexophagy. Heat shock protein 70 s mediates the translocation of the ubiquitin E3 ligase Stub1 (STIP1 Homology and U-Box Containing Protein 1) onto oxidatively-stressed peroxisomes to promote their selective ubiquitination and autophagic degradation. Artificially targeting Stub1 to healthy peroxisomes is sufficient to trigger pexophagy, suggesting a key role Stub1 plays in regulating peroxisome quality. We further determine that Stub1 mutants found in Ataxia patients are defective in pexophagy induction. Dysfunctional peroxisomal quality control may therefore contribute to the development of Ataxia.

Suggested Citation

  • Bo-Hua Chen & Yao-Jen Chang & Steven Lin & Wei Yuan Yang, 2020. "Hsc70/Stub1 promotes the removal of individual oxidatively stressed peroxisomes," Nature Communications, Nature, vol. 11(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-18942-3
    DOI: 10.1038/s41467-020-18942-3
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    Cited by:

    1. Kyla Germain & Raphaella W. L. So & Laura F. DiGiovanni & Joel C. Watts & Robert H. J. Bandsma & Peter K. Kim, 2024. "Upregulated pexophagy limits the capacity of selective autophagy," Nature Communications, Nature, vol. 15(1), pages 1-18, December.

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