Background: Parkinson’s disease is a progressive neurological disease that affects especially the older population. One hallmark of the disease is the loss of dopaminergic neurons in the midbrain. While other causes of Parkinson’s disease are still unclear, the loss of mitochondrial functions is a key feature of the disease. A key molecule for the correct function of mitochondria is Parkin. Defects in Parkin are linked to different subtypes of Parkinson‘s disease and other essential cellular protein quality control mechanisms. Recently, it was shown that the ubiquitination activity of Parkin regulates mitochondrial-ER contact sites (MERCS).
Objectives: The post-doctoral fellow will work on the characterization of the MERCS protein interactome in neurons using mass spectrometry-based proteomics.
Training and research environment: The proteomics of cellular signaling group is highly international, with members from France, Portugal, the USA, Brazil, Germany, Belgium, Lebanon, Pakistan and Poland. The group is part of the Department of Infection and Immunity, and its research focuses on regulation by post-translational modifications and changes in the protein-protein interactome using mass spectrometry-based techniques. The post-doctoral researcher will work on a DFG/FNR-funded project targeted at identifying new components of the MERCS. The project is a close collaboration with the laboratory of Anne Grünewald (University of Luxembourg) and Dajana Grossmann (University of Rostock, Germany).
Recent related references: Grossmann, D., et al. (2020). The Emerging Role of RHOT1/Miro1 in the Pathogenesis of Parkinson’s Disease. Front. Neurol. 11, 587. Grossmann, D., et al, (2023). Mitochondria-Endoplasmic Reticulum Contact Sites Dynamics and Calcium Homeostasis Are Differentially Disrupted in PINK1-PD or PRKN-PD Neurons. Mov. Disord. Grünewald, A., et al. (2019). New insights into the complex role of mitochondria in Parkinson’s disease. Prog. Neurobiol. 177, 73–93.
Key Skills, Experience and Qualifications
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