Peroxisomes are essential organelles required for proper cell function in all eukaryotic organisms. They participate in a wide range of cellular processes including the metabolism of lipids and generation, as well as detoxification, of hydrogen peroxide (H2O2). Therefore, peroxisome homoeostasis, manifested by the precise and efficient control of peroxisome number and functionality, must be tightly regulated in response to environmental changes. Due to the existence of many physiological disorders and diseases associated with peroxisome homoeostasis imbalance, the dynamics of peroxisomes have been widely examined. The increasing volume of reports demonstrating significant involvement of the autophagy machinery in peroxisome removal leads us to summarize current knowledge of peroxisome degradation in mammalian cells. In this review we present current models of peroxisome degradation. We particularly focus on pexophagy–the selective clearance of peroxisomes through autophagy. We also critically discuss concepts of peroxisome recognition for pexophagy, including signalling and selectivity factors. Finally, we present examples of the pathological effects of pexophagy dysfunction and suggest promising future directions.
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April 2016
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Cover Image
Endoplasmic reticulumendosome contact sites. This pseudo-colored electron microscopy image shows the formation of inter-organelle membrane contact sites between late endosomes (magenta) and the endoplasmic reticulum (ER; green). This tethering results from the interaction between two ER-anchored proteins (VAP-A and VAP-B) and the late endosomeanchored protein STARD3NL. Mitochondria: brown; nucleus: blue. For further details see pp. 493-498. Image kindly provided by Fabien Alpy. - PDF Icon PDF LinkTable of Contents
Review Article|
April 11 2016
Autophagic degradation of peroxisomes in mammals
Katarzyna Zientara-Rytter;
Katarzyna Zientara-Rytter
*Section of Molecular Biology, Division of Biological Sciences, University California, San Diego, CA 92093-0322, U.S.A.
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Suresh Subramani
Suresh Subramani
1
*Section of Molecular Biology, Division of Biological Sciences, University California, San Diego, CA 92093-0322, U.S.A.
1To whom correspondence should be addressed (email ssubramani@ucsd.edu).
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Publisher: Portland Press Ltd
Received:
January 27 2016
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2016 Authors; published by Portland Press Limited
2016
Biochem Soc Trans (2016) 44 (2): 431–440.
Article history
Received:
January 27 2016
Citation
Katarzyna Zientara-Rytter, Suresh Subramani; Autophagic degradation of peroxisomes in mammals. Biochem Soc Trans 15 April 2016; 44 (2): 431–440. doi: https://doi.org/10.1042/BST20150268
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