On Friday (30.10) we will host Professor Andreas Ladurner. His lecture will be entitled: "A metabolite-gated conformational switch in ChREBP–14-3-3 controls sugar tolerance". The lecture will take place on FRIDAY at 3 p.m. in the CN lecture hall and it will be followed by a get together.

Professor Andreas Ladurner is a biochemist and internationally recognized expert in chromatin biology, serving as Professor and Chair of Physiological Chemistry at the Biomedical Center of Ludwig Maximilian University of Munich (LMU), Germany. His research investigates the molecular mechanisms underlying chromatin plasticity and how post-translational modifications, cellular metabolites and chromatin-remodelling machinery regulate gene expression and cellular adaptation. His group focuses on PARP1-dependent ADP-ribosylation signalling, chromatin remodelling in DNA damage responses and regulation of transcription by metabolite-sensing proteins. Prof. Ladurner obtained his PhD in Chemistry from the University of Cambridge in 2000 under the supervision of Sir Alan Fersht, followed by postdoctoral research with Robert Tjian at the Howard Hughes Medical Institute, University of California, Berkeley. He subsequently led a research group at the European Molecular Biology Laboratory (EMBL) in Heidelberg from 2003 to 2011 before joining LMU as a full professor in 2010. He is also the co-founder and Chief Scientific Officer of Eisbach Bio, a biotechnology company developing therapeutic approaches targeting molecular mechanisms in cancer. His seminar will be followed by a get-together in the exhibition hall.

Abstract:

How do our cells sense sugar and translate its availability into changes in gene activity? We will report on our discovery that the human transcription factor ChREBP controls sugar and fat metabolism by functioning as a molecular sensor together with its partner protein 14-3-3. Two metabolites, glucose-6-phosphate and AMP, bind this complex but trigger different structural changes, switching its activity on or off, respectively. We show how this conserved molecular mechanism controls gene expression and enables animals to tolerate sugar-rich diets, revealing a fundamental connection between metabolism, gene regulation, sugar tolerance and obesity.