Meie uurimistöö on seotud selliste molekulaarsete mehhanismide väljaselgitamisega, mis põhjustavad mutatsioonisageduse suurenemist stressis olevates bakterites. Täpsemalt seisneb meie uurimistöö erinevate DNA polümeraaside ja DNA-s tekkinud vigu parandavate süsteemide tööd koordineerivate mehhanismide selgitamises perekonda Pseudomonas kuuluvates bakterites.
Mutagenic mechanisms in stressed microorganisms differ from those characterized in actively growing cells. These mechanisms are important in the development of antibiotic resistance mutations, colonization of new bacterial hosts, pathogenesis and evolution of microorganisms. In stressed bacterial cells, DNA synthesis may become more erroneous because of the induction of error-prone DNA polymerases, resulting in a situation in which DNA repair systems are unable to cope with increasing amounts of DNA lesions. Transposition may also increase genetic variation. The aim of our research is to study molecular mechanisms of stress-induced mutagenesis in a group of bacteria belonging to genus Pseudomonas. These bacteria are able to colonize many different environments, including soil and water, but also plant and animal tissues. We are studying the role of error-prone DNA polymerases and efficiency of DNA repair pathways on stress-induced mutagenesis in Pseudomonas bacteria. We are also elucidating mechanisms controlling frequency of transposition. This research would be in importance to understand basic mechanisms of evolution of microorganisms, genetic adaptation of plant and animal pathogens during host invasion, and this knowledge in turn would be useful to find new therapeutic targets in pathogenic bacteria.