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A03 - Ubiquitin-dependent regulation of mitochondrial fusion

Mafalda Escobar-Henriques
CECAD Research Center/Institute for Genetics
University of Cologne

Phone: +49 - 221 / 478 84257         
E-mail: MafaldaEscobar@uni-koeln.de
For more information and contact please visit the ESCOBAR LAB.

Mitochondrial fusion is essential to maintain mitochondrial plasticity and cellular respiration. It depends on conserved dynamin-related proteins in the outer membrane, termed Fzo1 in yeast and Mfn1/2 in mammals, whose loss triggers neurodegeneration in disease. The activity of mitofusins is regulated by ubiquitylation both in yeast and mammals. We have identified two Fzo1 ubiquitylation pathways that either promote or inhibit fusion, thus providing a maximum response capacity to cellular needs and prevent disease. In this project, we want to unravel the molecular mechanisms governing Fzo1 ubiquitylation and its implications in health and disease.

Latest publications
Simões, T., Schuster, R., den Brave, F., Escobar-Henriques, M. (2018). Cdc48 regulates a deubiquitylase cascade critical for mitochondrial fusion. Elife 7. pii: e30015. doi: 10.7554/eLife.30015. [Epub ahead of print]

Escobar-Henriques, M. (2014). Mitofusins: ubiquitylation promotes fusion. Cell Res. 24, 387-388.