Rate My Professor Marc-David Ruepp

Marc-David Ruepp is Professor of RNA Biology and Molecular Neurodegeneration in the Department of Basic & Clinical Neuroscience at King’s College London and Group Leader at the UK Dementia Research Institute (UK DRI). A ribonucleic acid biochemist, his research centers on gene expression in health and disease, particularly dysfunctional RNA metabolism contributing to selective neuronal death in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). He received his PhD in 2009 from the Graduate School of Cellular and Biomedical Sciences, University of Bern, Switzerland. Ruepp habilitated at the Faculty of Science, University of Bern, earning his Venia Docendi in RNA biology in 2018. He launched his independent career as Junior Group Leader in 2014 in the Department of Chemistry and Biochemistry at the University of Bern. In 2018, he joined King’s College London as Senior Lecturer and the UK DRI as Group Leader, promoted to Reader in 2022 and Professor in 2025. He serves as a Fellow of the UK DRI and Academic Mentor for PhD students in his department.

Ruepp's laboratory employs advanced techniques including CRISPR, stem cell models, next-generation sequencing, and microscopy to study RNA-binding proteins like FUS and TDP-43, mitochondrial dysfunction, miRNA deregulation, nuclear pore interactions, and local mRNA translation in neurons. Key publications include “Single-cell RNA-sequencing reveals early mitochondrial dysfunction unique to motor neurons shared across FUS- and TARDBP-ALS” (Schweingruber et al., Nature Communications, 2025), “Aberrant interaction of FUS with the U1 snRNA provides a molecular mechanism of FUS induced amyotrophic lateral sclerosis” (Jutzi et al., Nature Communications, 2020), “Minor intron splicing is regulated by FUS and affected by ALS-associated FUS mutants” (Reber et al., EMBO Journal, 2016), “Mutations in FUS lead to synaptic dysregulation in ALS-iPSC derived neurons” (Shum et al., Stem Cell Reports, 2024), and “A multimodal screening platform for endogenous dipeptide repeat proteins in C9orf72 patient iPSC neurons” (Hölbling et al., Cell Reports, 2025). He has obtained grants from the UK DRI and Motor Neurone Disease Association for research on ALS pathomechanisms, therapeutic RNA trans-splicing, and nuclear-synaptic signaling.