YEAST 2017

28th International Conference on Yeast Genetics and Molecular Biology (ICYGMB)

August 27 – September 1, 2017
Prague, Czech Republic

Paper ID: 329

Regulation of mitophagy by (de-)ubiquitylation

Behrendt Christina, Reichert Andreas S.

Heinrich Heine University Düsseldorf, Medical Faculty (Germany)


The selective degradation of mitochondria, termed mitophagy, is an evolutionarily conserved process. There is cumulating evidence that this process is linked to numerous human disorders including Morbus Parkinson. One pathogenic mechanism proposed is that the removal of damaged mitochondria is impaired promoting neurodegeneration. Mitophagy can be divided mechanistically into two principal ways: a receptor -mediated and an ubiquitin- mediated pathway. Mutations in genes such as PINK1 or PARKIN that are essential for the ubiquitin-mediated pathway in mammalian cells are known to cause Morbus Parkinson. Recent research suggest that an ubiquitin-mediated mitophagy pathway may also exist in baker’s yeast. We addressed the role of all three non-essential ubiquitin genes (UBI1, UBI2, UBI4) in different types of selective autophagy in Saccharomyces cerevisiae. We disect how mitophagy depends on these genes and how this is possibly linked to the deubiquitinase complex Ubp3/Bre5. We further identified an outer membrane protein as a novel player required for mitophagy. In summary, we identified a mitophagy pathway in yeast, which depends on mitochondrial protein ubiquitylation and which is dynamically regulated by ubiquitylation and Ubp3-dependent deubiquitylation.

Parkinson, Mitophagy, Ubiquitinylation, Deubiquitinase, Mitochondria
Presented as:
  Oral presentation [S6-3] in S6 Cell cycle and cell fate

Institute of Microbiology

YEAST 2017
28th International Conference on Yeast Genetics and Molecular Biology (ICYGMB)

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