The chemical structures and accumulation kinetics of several major soluble as well as wall-bound,
alkali-hydrolyzable compounds induced upon
infection of Arabidopsis thaliana leaves with Pseudomonas syringae pathovar tomato were established. All identified accumulating products were structurally related to
tryptophan. Most prominent among the soluble substances were
tryptophan, beta-d-glucopyranosyl
indole-3-carboxylic acid, 6-hydroxyindole-3-carboxylic
acid 6-O-beta-d-glucopyranoside, and the indolic phytoalexin
camalexin. The single major accumulating wall component detectable under these conditions was
indole-3-carboxylic acid. All of these compounds increased more rapidly, and
camalexin as well as
indole-3-carboxylic acid reached much higher levels, in the incompatible than in the compatible P. syringae/A. thaliana interaction. The only three prominent phenylpropanoid derivatives present in the soluble extract behaved differently. Two
kaempferol glycosides remained largely unaffected, and
sinapoyl malate decreased strongly upon
bacterial infection with a time course inversely correlated with that of the accumulating
tryptophan-related products. The accumulation patterns of both soluble and wall-bound compounds, as well as the
disease resistance phenotypes, were essentially the same for infected wild-type and tt4 (no
kaempferol glycosides) or fah1 (no
sinapoyl malate) mutant plants. Largely different product combinations accumulated in wounded or senescing A. thaliana leaves. It seems unlikely that any one of the
infection-induced compounds identified so far has a decisive role in the resistance response to P. syringae.