Abstract
M.Sc.
Field grown plants are constantly challenged with a variety of stressful factors, such as high temperatures,
drought and pathogen infection that adversely affect crop production and quality. These stresses seldom
occur as single entities in plants and in warm climates, heat stress is often a common dominator in
combinatorial stress. The heat shock (HS) response in plants has priority over other stress responses,
including the pathogen-induced stress response. Activation of the HS response prevents the normal plant
defence strategy, leaving the plant vulnerable to pathogen attack. However, prior exposure to elevated
temperatures confers protection from subsequent, otherwise lethal, temperatures (thermotolerance) and a
variety of other stress conditions including heavy-metals, chilling injury and certain pathogens (cross
tolerance). In general, litterature supports a central role for heat shock proteins (HSP), in particular the 70
kDa HSP (Hsp70), in thermotolerance. Incompatible host-pathogen interactions lead to the activation of
an array of defence mechanisms, including the promotion of phenylpropanoid metabolism. Phenylalanine
ammonia-lyase is a key regulator of this metabolic pathway, influencing the production of salicylic acid,
lignin and phytoalexins among other essential defence products. In this study it was hypothesised that
prior exposure to non-lethal HS confers protection from subsequent heat-related suppression of the
phenylpropanoid pathway, induced as a defence mechanism during an incompatible plant-pathogen
interaction. This hypothesis was verified by analysing the effect of thermotolerance on pathogen-related
stimulation of PAL promoter activity, enzyme activity and lignin deposition. The tomato, Lycopersicon
esculentum cultivar UC82B and Ralstonia solanacearum, the causative agent of bacterial wilt, were used
as host-pathogen model. Specific objectives in the study were: (1) Development of PAL promoter-GUS
reporter transformed Lycopersicon esculentum. (2) Establishment of a thermotolerance protocol that
ensures optimal Hsp70 levels at subsequent HS. (3) Evaluation of the influence of prior heat treatment on
phenylpropanoid metabolism after exposure to HS in combination with Ralstonia solanacearum. Results
obtained support the hypothesis indicating that thermotolerance protects phenylpropanoid metabolism, in
particular PAL promoter and enzyme activity, and to a certain extent lignin production, induced by avirulent
Ralstonia solanacearum during a second severe HS. In contrast, HS without a prior heat treatment,
suppressed phenylpropanoid metabolism. The protective potential of prior heat treatment during
subsequent infection under hyperthermic conditions support the application of HSP in the development of
novel plant protection strategies.