Inner mitochondrial membrane protein Prohibitin 1 mediates Nix-induced, Parkin-independent mitophagy

Inner mitochondrial membrane protein Prohibitin 1 mediates Nix-induced, Parkin-independent mitophagy

Autophagy of damaged mitochondria, called mitophagy, is an important organelle quality control process involved in the pathogenesis of inflammation, cancer, aging, and age-associated diseases. Many of these disorders are associated with altered expression of the inner mitochondrial membrane (IMM) pr...

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Bibliographic Details
Published in:Scientific reports Vol. 13; no. 1; p. 18
Main Authors: Alula, Kibrom M., Delgado-Deida, Yaritza, Callahan, Rosemary, Till, Andreas, Underwood, Lucia, Thompson, Winston E., Souza, Rhonda F., Dassopoulos, Themistocles, Onyiah, Joseph, Venuprasad, K., Theiss, Arianne L.
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 02-01-2023
Nature Publishing Group
Nature Portfolio
Subjects:
631/80/39
631/80/642/333
692/4020/2741/520
Aging
Apoptosis
Autophagy
Bowel disease
Crohns disease
Epithelial cells
Epithelium
Esophagus
Homeostasis
Humanities and Social Sciences
Inflammation
Localization
Medicine
Membrane proteins
Membrane Proteins - metabolism
Mitochondria
Mitochondria - metabolism
Mitochondrial DNA
Mitochondrial Membranes - metabolism
Mitochondrial Proteins - metabolism
Mitophagy
multidisciplinary
Parkin protein
Prohibitin
Prohibitins
Proteins
Quality control
Reactive oxygen species
Reactive Oxygen Species - metabolism
Science
Science (multidisciplinary)
Ubiquitin-Protein Ligases - metabolism
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Summary:Autophagy of damaged mitochondria, called mitophagy, is an important organelle quality control process involved in the pathogenesis of inflammation, cancer, aging, and age-associated diseases. Many of these disorders are associated with altered expression of the inner mitochondrial membrane (IMM) protein Prohibitin 1. The mechanisms whereby dysfunction occurring internally at the IMM and matrix activate events at the outer mitochondrial membrane (OMM) to induce mitophagy are not fully elucidated. Using the gastrointestinal epithelium as a model system highly susceptible to autophagy inhibition, we reveal a specific role of Prohibitin-induced mitophagy in maintaining intestinal homeostasis. We demonstrate that Prohibitin 1 induces mitophagy in response to increased mitochondrial reactive oxygen species (ROS) through binding to mitophagy receptor Nix/Bnip3L and independently of Parkin. Prohibitin 1 is required for ROS-induced Nix localization to mitochondria and maintaining homeostasis of epithelial cells highly susceptible to mitochondrial dysfunction.
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ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-022-26775-x