We are a team of scientists focusing our interests on bacteria of the genus Mycobacterium. We are motivated by the current threat because many mycobacteria are pathogens, most notably Mycobacterium tuberculosis, which causes tuberculosis. We are looking for new anti-mycobacterial drugs and diagnostic methods, we study the virulence of mycobacteria and their interaction with the host. We conduct our research from a single chemical molecule to bacterial ecosystems. We focus our research on the biology of the mycobacterial cell (DNA repair mechanisms, tRNA maturation, transcription, signal transduction, sterol metabolism and cell wall biosynthesis) and genetic variability in the population.
In our research, we routinely use site-directed mutagenesis to construct genetically modified mycobacteria. Our team has a significant collection of M. smegmatis and M. tuberculosis mutants, which we willingly share in implementing joint research projects. We use molecular biology methods, including high-throughput sequencing of genomes and transcriptomes, molecular cloning, expression of recombinant proteins, and their analysis in in vitro tests. In research on the virulence of Mycobacterium tuberculosis, we also use in vivo methods, most often using cell cultures. We use in silico methods to analyze genetic variation. We have modern equipment that allows us to screen potential antibacterial compounds.
Our most important achievements were to show that (i) M. tuberculosis is capable of accumulating and utilizing cholesterol, (ii) cholesterol oxidase is a virulence factor of M. tuberculosis, and a functional cholesterol utilization system is essential for intracellular survival of mycobacteria in host phagocytic cells, (iii ) trehalose monomycolate flipase is a molecular target for benzimidazole derivatives in M. tuberculosis and M. abscessus (iv) identification of tuberculosis ligands for elements of the host immune system, (v) AEP family primases are involved in BER type DNA repair.