Speaker
Description
Horizontal gene transfer (HGT) is a fundamental process in bacterial evolution and is typically driven by mobile genetic elements, with conjugative plasmids one of the most significant sources of bacterial HGT. In addition to functional traits such as antibiotic resistance, plasmids also frequently encode homologs of bacterial regulators that can dramatically change the expression of chromosomally-encoded bacterial traits, a process known as plasmid-chromosome crosstalk (PCC). We recently characterised two PCC regulators from the megaplasmid pQBR103 that subvert ecologically relevant pathways in the soil bacterium Pseudomonas fluorescens. These plasmid-borne regulators appear similar to host proteins, but act in strikingly different ways, subverting host regulation and behaviour to benefit plasmid transmission. For example, RsmQ is a homolog of the bacterial translational regulator RsmA that disrupts the host Gac/Rsm pathway, influencing chemotaxis, metabolism and plasmid conjugation rate. Meanwhile, the plasmid-borne ParB-mimic ParQ functions as a transcriptional regulator of bacterial motility and chemotaxis. The RsmQ and ParQ regulons interact with one another and with the host cyclic-di-GMP network, with deletions in specific diguanylate cyclase genes recovering motility defects associated with plasmid carriage. pQBR103 apparently contains multiple putative PCC regulatory proteins, whose function is under active investigation in my lab. The intersection of plasmid and bacterial signalling driven by PCC regulators promotes plant colonisation, sessility and biofilm formation, traits that in turn support community transmission of the pQBR103 plasmid. Together, these findings expand our knowledge of the regulatory mechanisms underpinning HGT, and have broad implications for our understanding of how plasmids influence microbial communities.
