Prof. Dr. Franziska Faber

Enteric infections and their clinical outcome are often associated with underlying microbial dysbiosis. Clostridioides difficile – being a leading cause of antibiotic-associated diarrhea – is a prime example. Therefore, a mechanistic understanding of virulence regulation in the context of pathogen-commensal interactions is paramount for the development of novel therapeutics.
The production of toxins and the ability to form antibiotic-resistant spores are the major virulence factors in C. difficile that contribute to significant morbidity and mortality and to high recurrence rates in patients. Their production is tightly regulated by metabolic signals whose abundance and composition throughout the infection cycle is shaped by the gut microbial community.

In our lab, we combine deep RNA-sequencing based approaches with RNA biology, biochemical, genetic and microbiology techniques to discover and mechanistically characterize non-coding RNAs and their RNA-binding protein partners involved in virulence gene regulation.
We are also interested in how the activities of these regulators is shaped by microbial and host signals. To better understand this cross-talk, we take a bottom-up approach by studying individual pathogen-commensal interactions integrating microbiology, genetic, advanced cell culture and metabolomics approaches.

The overarching goal of the Faber group is to identify and functionally characterize novel RNA-based mechanisms of virulence regulation that can be exploited as therapeutic targets.