We are interested in the molecular mechanisms that control cell-to-cell heterogeneity in pathogen populations.

Our group has a long history of exploring different next-generation-sequencing (NGS)-based approaches such as single-cell RNA-seq, ATAC-seq, ChIP-seq, ribosome-profiling and Hi-C to elucidate links between chromatin structures, genome architectures and gene expression. Combining these NGS-based approaches with super-resolution microscopy, various microfluidics set-ups and sophisticated image-activated cell-sorting approaches, our lab hopes to investigate at the single-cell level how pathogens benefit from cell-to-cell heterogeneity.

As a model to study cell-to-cell heterogeneity, we study antigenic variation in Trypanosoma brucei, a unicellular parasite responsible for sleeping sickness in humans and nagana in cattle.

Throughout its life cycle, T. brucei remains extracellular. As a consequence, in its mammalian host, the parasite is readily recognized by the host immune system. Elimination is avoided by the parasite’s ability to change the composition of its surface coat, a strategy referred to as – antigenic variation.

Our key goal is to understand how changes in chromatin structures and genome architecture influence antigenic variation at the single-cell level.

Chromatin organization, genome architecture, antigenic variation, single-cell biology

Trypanosoma brucei