Protection of phenylpropanoid metabolism by prior heat treatment in Lycopersicon esculentum exposed to Ralstonia solanacearum

Heat shock inhibits pathogen-induced resistance mechanisms in incompatible plant hosts, leaving them vulnerable to pathogen attack. Prior exposure of organisms to non-lethal heat induces heat shock proteins and acquired thermotolerance to otherwise lethal high temperatures. The phenylpropanoid pathway is a target of heat-related inhibition but it is unknown whether thermotolerance protects this pathway or its key regulator, phenylalanine ammonia-lyase (EC 4.3.1.5, PAL). It was hypothesised that prior exposure to a heat shock pulse to induce the accumulation of heat shock proteins, specifically the 70-kDa heat shock protein (Hsp70 – inducible/Hsc70 – constitutive), would protect phenylpropanoid metabolism from heat-induced inhibition. The tomato, Lycopersicon esculentum L. cv. UC82B, transformed with PAL2-GUS, and Ralstonia solanacearum, biovar II, were used as incompatible host-pathogen model. A prior heat shock pulse induced significant accumulation of Hsp70/Hsc70 and enhanced cell viability. This protected the pathogen-activated phenylpropanoid pathway (PAL2-GUS activity, PAL enzyme activity, lignin deposition) from heat-induced inhibition and promoted cell survival after a subsequent prolonged heat shock. This study suggests phenylpropanoid metabolism as a target of Hsp70/Hsc70-related protection of the resistance response activated in tomato against avirulent strains of Ralstonia solanacearum from heat-induced inhibition during a concomitant heat shock.