Phytoalexins and polar metabolites from the oilseeds canola and rapeseed:: Differential metabolic responses to the biotroph Albugo candida and to abiotic stress

The metabolites produced in leaves of the oilseeds canola and rapeseed (Brassica rapa L.) inoculated with either different races of the biotroph Albugo candida or sprayed with CuCl2 were determined. This investigation established consistent phytoalexin (spirobrassinin, cyclobrassinin, and rutalexin) and phytoanticipin (indolyl-3-acetonitrile, arvelexin, caulilexin C, and 4-methoxyglucobrassicin) production in canola and rapeseed in response to both biotic and abiotic elicitation. In addition, a wide number of polar metabolites were isolated from infected leaves, including six new phenylpropanoids and two new flavonoids. The extractable chemical components of zoosporangia of A. candida and the anti-oomycete activity of phytoalexins were determined as well. Overall, the results suggest that during the initial stage of the interaction, leaves of B. rapa have a similar response to virulent and avirulent races of A. candida, with respect to the accumulation of chemical defenses. After this stage, despite the higher phytoalexin concentration, the "compatible" races could overcome the plant defense system for further infection, but growth of the "incompatible" races was inhibited. Since results of bioassays showed that cyclobrassinin and brassilexin were more inhibitory to A. candida than rutalexin, the apparent redirection of the phytoalexin pathway towards rutalexin, avoiding cyclobrassinin and brassilexin accumulation might be caused by the pathogen. Alternatively, A. candida might be able to detoxify both cyclobrassinin and brassilexin, similar to necrotrophic plant pathogens. Overall, the correlation between phytoalexin production in infected or stressed leaves and the outcome of the plant-pathogen interaction suggested that A. candida was able to elude the plant defense mechanisms by, for example, redirecting the phytoalexin biosynthetic pathway. (C) 2007 Elsevier Ltd. All rights reserved.