Ihre Aufgaben

• Investigate the pathophysiology of LRRK2-mediated Parkinson’s disease using primary cell culture, biochemical experiments, and live-imaging microscopy.
• Design and conduct experiments.
• Record, analyze, and present experimental data.
• Publication of results in international, peer-reviewed journals.

Ihre Qualifikationen

• PhD in biology, neuroscience, or equivalent discipline.
• Willingness to learn about new techniques and scientific fields, intrinsic motivation and independency to contribute new ideas to the project.
• Team player and openness for collaboration.
• Experience in fluorescence microscopy, cellular biology, and biochemistry

Wir bieten

• Interesting job in a motivated and open-minded young team.
• Training in state of the art live-imaging microscopy.
• Careful and qualified training and support for the new challenge.
• Work on unravelling the pathophysiology of a devastating neurodegenerative disease currently without causal treatment options.
• Salary according to the German salary scale TV-L E 13

Einleitungstext
The research group ‘Cell Biology of Neurodegeneration’ headed by Dr. C. A. Boecker (m) is offering a position for a Postdoc (f/m/d).
We are looking for a Postdoc to join our team and contribute to a fully funded research pproject investigating the role of LRRK2 in the pathogenesis of Parkinson´s disease. The postition is funded by the Michael J. Fox Foundation. Earliest starting date possible is October 1st, 2025.
In collaboration with the groups of Sabine Hilfiker (Rutgers University, USA) and Luis Bonet-Ponce (The Ohio State University, USA), we will decipher how hyperactive LRRK2 kinase activity disrupts the intracellular pathways of axonal autophagosome transport, ciliogenesis/centriole cohesion and lysosomal membrane dynamics.
LRRK2 mutations are the most common genetic cause of Parkinson´s disease and lead to pathogenic hyperactivation of LRRK2 kinase. This results in hyperphosphorylation of RAB proteins and interferes with the above processes. Although these cellular deficits are all mediated by similar phospho-RAB effector protein interactions, it remains unclear whether they share a common core mechanism. In this collaborative project, we will determine whether the effects of LRRK2 are cell type-specific, address the interdependence of autophagosome, ciliogenesis/centriole cohesion and lysosomal dynamics alterations, and determine common versus pathway-specific molecular mechanisms downstream ofphospho-RAB effector recruitment.

Please refer the Job description for details