Strains of methicillin-resistant Staphylococcus aureus (MRSA), coagulase-negative staphylococci (CNS), and vancomycin-resistant enterococci (VRE) that are resistant to multiple antimicrobial agents, are a major cause of hospital-acquired infections around the world and are responsible for significant morbidity and mortality. These Gram-positive pathogens commonly contain multiresistance plasmids that encode partitioning systems, which increase their segregational stability. Such systems therefore contribute to the prevalence and spread of these plasmids, and effectively maintain resistance even in the absence of selection. Three types (I-III) of partitioning systems are recognised based on centromere structure and type of motor/DNA binding protein.

We have identified putative Type Ib partitioning systems on resistance plasmids from clinical staphylococcal and enterococcal isolates, which contain candidate centromere-like site(s), and parA and parB genes that are predicted to encode a deviant Walker ATPase motor protein and a ribbon-helix-helix DNA binding protein, respectively. Subsequently, we have shown that these partitioning systems, when cloned into mini-replicons, confer enhanced segregational stability in their respective hosts. Furthermore, in context of the staphylococcal system, we have shown that the putative ParB protein regulates par operon transcription and that a ParA-GFP fusion protein, which is functional in the absence of wild-type ParA, localises to the nucleoid; we are also currently examining the cellular localisation of other par system components.