Water stress alters aphid-induced glucosinolate response in Brassica oleracea var. italica differently

Abstract

Glucosinolates (GS) are the main secondary metabolites in brassicaceous plants that play an important role in plant defense and plant–insect communication. GS biosynthesis in plants and their accumulation may be influenced by biotic and abiotic stressors from the environment. In the present study, GS levels in broccoli plants, Brassica oleracea var. italica Plenck, grown under different water status conditions of soil—well-watered, drought and waterlogged—were determined after two aphid species, the specialist Brevicoryne brassicae (L.) and the generalist Myzus persicae (Sulzer), had fed on them for 7 days. High-performance liquid chromatography analysis revealed that GS levels were significantly induced after B.brassicae had fed on B. italica plants grown for 2 weeks under the various water status conditions. No significant differences were determined between GS induction in the three treatments. In contrast, the induction of GS after M. persicae had fed on the plants depended greatly on water stress levels. GS content in well-watered plants increased more significantly than in plants grown under drought conditions. Feeding by M. persicae did not increase GS levels when plants were grown under waterlogged conditions. The lowest plant growth were found in M. persicae-infested plants for all three water treatments, and measurements of GS showed that the induction of GS by M. persicae decreased in line with the reduction in infested plant growth. GS induction by B. brassicae did not alter remarkably following change in plant growth under water stress. Only one of the five glucosinolates detected, the aliphatic GS 4-methylsulfinylbutyl, remained unchanged after feeding of both, M. persicae and B. brassicae, on plants under water stress. Variation in GS levels was mainly observed for the induction of indolyl GS due to aphid herbivory, but changes in indol-3-ylmethyl GS were not always consistent with the induction of other indolyl GS.