Quorum sensing using N-acyl homoserine lactone (N-AHL) signal molecules is a cell density-dependent mechanism which allows bacterial cells to co-ordinate their behaviour in concern with their own population size. Previous studies have indicated that the pathogenic fungus Gaeumannomyces graminis var. tritici (Ggt) secretes a homoserine lactone that promotes gene expression in the potential biocontrol bacterium Pseudomonas corrugata. The aim of this thesis was therefore to investigate the role of N-AHL signalling in interactions between these two organisms. It was demonstrated that Ggt does not produce an N-AHL signal molecule or similar autoinducer capable of causing the reported increased transcription in P. corrugata. P. corrugata however was confirmed to produce an N-AHL signal molecule, and it was decided to elucidate this system to determine its possible role in expression of virulence/pathogenicity genes. aA gene was identified from the P. corrugata genome with significant homology to the LuxI family of AHL synthases. This was confirmed experimentally to produce multiple N-AHL signal molecules and the gene termed 'pcoI'. A putative transcriptional activator was also identified and termed 'pcoR', but was not required for production of N-AHL. Sequence analysis revealed close homology to Sa1A, a newly identified regulatory required for virulence and toxin production in P. syringae. Both genes were demonstrated to be involved in Ggt suppression in vitro. This work has provided a glimpse into the hierarchy and complex nature of signal pathways regulating virulence/pathogenicity in P. corrugata. Understanding the mechanisms through which the biocontrol of plant disease occurs is critical to the eventual improvement and wider use of biocontrol methods. In addition, the information from this study may prove beneficial for the manipulation of parameters affecting pathogenesis of P. corrugata and for the eventual control of plant disease.