WEHI Ubiquitin Signalling Centre special seminar hosted by David Komander and Catharina Kueng

Prof. Dr. rer. nat Angelika Harbauer

MPI für Biologische Intelligenz and Technical University Munich (TUM), Germany

PINK1 biology in neurons - logistics, contacts and protein translation

Davis Auditorium

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Including Q&A session

Please note this presentation will not be recorded

Prof. Harbauer studied Molecular Medicine at the Universität of Freiburg. She did her PhD thesis at the local Institute for biochemistry and molecular biology in the group of Prof. Meisinger working on the regulation of mitochondrial protein import.  She continued her studies as a post-doctoral fellow in the lab of Prof. Tom Schwarz at the Harvard Medical School, Boston, where she explored mitochondrial quality control in axons. Since September 2019 Prof. Harbauer is a Max Planck Research Group Leader at the MPI for Biological Intelligence in Martinsried. At the same time, she holds an appointment as a tenure-track professor for “Neurons and Metabolism” at the TU Munich.

Local maintenance of mitochondria is a crucial mechanism to counteract insults to this key organelle in neurons. A central role in mitochondrial quality control is played by the Parkinson-related mitochondrial kinase PINK1, whose mRNA is transported in neurons by mitochondrial hitch-hiking to allow the localized production of the mitochondrial quality sensor PINIK1.Our research has shown that local translation of PINK1 requires a concerted interplay between three organelles. While mitochondria carry the PINK1 mRNA and receive the final protein product, the mRNA can be untethered due to disassembly of the RNA anchoring complex downstream of insulin signaling. The mRNA then relocates to the endolysosomal compartment, whose degradative function is needed for PINK1 synthesis. The endoplasmic reticulum at this contact site contributes membrane-tethered chaperones, enabling the transfer of the newly synthesized PINK1 precursor to mitochondria in the ER-SURF pathway. The entirety of this complex multi-organelle mechanism is necessary for PINK1’s ability to demarcate damaged mitochondria and target them for mitophagy in neurons.

All welcome!