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Dynamic survey of mitochondria by ubiquitin

Mafalda Escobar‐Henriques, Thomas Langer

Author Affiliations

  1. Mafalda Escobar‐Henriques*,1 and
  2. Thomas Langer1,2
  1. 1Institute for Genetics Centre for Molecular Medicine (CMMC) Cologne Excellence Cluster on Cellular Stress Responses in Aging‐Associated Diseases (CECAD) University of Cologne, Cologne, Germany
  2. 2Max‐Planck‐Institute for the Biology of Aging, Cologne, Germany
  1. *Corresponding author. Tel: +49 221 470 4295; Fax: +49 221 470 6749; E‐mail: Mafalda.Escobar{at}uni-koeln.de

Abstract

Ubiquitin is a post‐translational modifier with proteolytic and non‐proteolytic roles in many biological processes. At mitochondria, it performs regulatory homeostatic functions and contributes to mitochondrial quality control. Ubiquitin is essential for mitochondrial fusion, regulates mitochondria‐ER contacts, and participates in maternal mtDNA inheritance. Under stress, mitochondrial dysfunction induces ubiquitin‐dependent responses that involve mitochondrial proteome remodeling and culminate in organelle removal by mitophagy. In addition, many ubiquitin‐dependent mechanisms have been shown to regulate innate immune responses and xenophagy. Here, we review the emerging roles of ubiquitin at mitochondria.

See the Glossary for abbreviations used in this article.

EMBO Reports (2014) 15, 231–243

  • Received November 13, 2013.
  • Revision received January 16, 2014.
  • Accepted January 20, 2014.

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