Abstract
The pathogenicity of the bacterium Erwinia carotovorasubsp. atroseptica, which causes potato soft rot, is triggered by short oligogalacturonates released by enzymic degradation of plant cell wall pectin. In the first stage unsaturated digalacturonate (uDG), produced by the action of pectate lyases, is degraded by oligogalacturonide lyase (OGL) to keto-deoxyuronate (DKI). The OGL encoding gene from E. carotovoraand the corresponding recombinant enzyme were characterized. Measuring the changes in plant cell viability and tissue maceration during soft rot pathogenesis in tissue slices of sprouting potato tubers, it was observed that exposure to uDG and DKI, produced by recombinant OGL, killed up to 30% of the plant cells over a period of 16h. This protected the tissue against maceration by E. carotovorasubsp. atroseptica. Endogenous OGL activity was detected in extracts from sprouting tubers where it may be involved in the conversion of uDG into cell toxic compounds. The results indicate that an additional function of small, diffusable digalacturonates is to induce plant cell death during the rotting process, thus contributing to defence reactions against E. carotovorasubsp. atroseptica.
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