Our group is interested in understanding how mutations occur in cells of bacteria, and how cells avoid mutagenesis with different repair strategies. We are also interested in understanding repair systems in humans, and how defects in these systems lead to cancer. We have extended our work to examine how antibiotics interact with different gene products in the cell, and are involved in defining genes that when knockout out result in increased sensitivity to antibiotics. The ultimate goal is to develop co-drugs that can be used to potentiate antibiotics to both lower the required dose, thus decreasing side-effects, and to overcome some of the antibiotic resistance generating mutations that occur in pathogens. We have detected new repair systems for oxidative damage in bacteria, and have charactered the human repair genes which are equivalent, and have made and studied knockout mice lacking these gene. We have exploited the strategy of examining mutator strains, those with higher mutation rates, to detect new repair systems in bacteria. We have found genes from other organisms that cause higher mutation rates in bacteria. We are extending this work to include genes from DNA extracted without cultivation from different microorganism communities.
