UMR CNRS 5557, Université Claude Bernard, Lyon 1, Bâtiment 741, 69622 Villeurbanne Cedex, France; 2Department of Biological and Biomedical Sciences, University of the West of England, Bristol BS16 1QY, UK

Background and objectives
Pseudomonas syringae pathovar pisi P. s. pisi) is the causal agent of pea bacterial blight. Differential interactions between strains of the pathovar and cultivars of pea lead to either disease symptoms (typified by water soaking) or resistance (typified by the hypersensitive response). The pattern of interactions may be interpreted in terms of a gene-for-gene (GFG) model involving six pairs of genes for avirulence (named A1 to A6) in the pathogen and resistance (named R1 to R6) in the plant. Seven races of P. s. pisi were defined according to this pattern [1]. Evolution of GFG interactions involving agricultural plants is influenced by the planting regimes and resistance allele frequencies. In this study, we investigated, through phylogenetic analyses, the evolution of the defined pea-related GFG races of P. s. pisi to establish the impact of the GFG structure on their diversification.

Results and conclusions
HrpL, an alternate sigma factor of the sigma 70 protein family is used to infer phylogenetic relationships among P. s. pisi. HrpL is shown to evolve orthologously and to be a good marker of the phylogenetic relationships among P. syringae. P. s. pisi is shown to be monophyletic and analysis of its radiation shows a diversification into three lineages: (I) a race 4A lineage, (II) a lineage corresponding to races 2, 3A and 6, and (III) a lineage corresponding to races 1, 3B, 4B, 5 and 7. Race 4A diverged early from the other two lineages. The P. s. pisi radiation seems to have emerged with selection of variants that became the agents of pea bacterial blight. Further selection events toward nonrecognition by pea then appear to have taken place: the race 4A appears to have emerged owing to the loss of several avirulence properties early in the evolution of this pathovar and the above lineages II and III appear to have diverged after changes in their avirulence properties and particularly the loss of the avirulence 4 phenotype.

1. Bevan JR, Taylor JD, Crute IR, Hunter PJ, Vivian A. 1995. Plant Pathology 44,98-108.