Abstract
Mutators are cells that have a higher mutation rate than the wild type. Such mutators have been extensively studied in bacteria, and this has led to the elucidation of a number of important DNA repair pathways, as well as revealing new pathways of mutagenesis. Repair defects in humans that lead to mutator phenotypes are responsible for a number of cancer susceptibilities. In some cases, these repair systems are the close counterparts of the equivalent bacterial repair system. Therefore, characterizing bacterial mutators and the repair systems that are deficient can aid in discovering the human homolog of these systems.