How are plants defending themselves from the outside intrusions?
Plants are constantly defending themselves against an array of assaults by pathogenic organisms. Glucosinolates (GSLs) and their hydrolysis products have been shown to play important roles in enabling formidable plant defenses. This review provides a comprehensive report of how indole and aliphatic GSLs mitigate incidences of plant pathogenesis. Seven economically important brassica pathogens were reviewed regarding their ability to disrupt proper plant functioning as well as the mechanisms by which GSLs and their hydrolysis products lower plant susceptibility to them. Future perspectives of the application of GSLs in plant pathogen resistance using advanced molecular techniques are also discussed.
Plant biochemical defense mechanism evolved overtime through phytochemical mediated strategies to adapt and overcome the antagonistic stress that may impair growth and reproduction. According to Dangl and Jones, the lack of mobile defender cells and somatic adaptive immune systems ensures that plant often relies on the innate immunity of individual cells and systemic signals emanating from infection sites to initiate and coordinate defense response.
The propagation of this response leads to effect beyond their site of initiation. Upon recognition of invading pathogens, Lehmann and Torres opined that host cells respond by producing and accumulating reactive oxygen species (ROS), which have been studied not only for their role in plant development but also for eliciting immunity. Although this sort of first response depends on the nature and severity of the pathogen and threat as well as the plant group. The multi-layered response system of the plant, which depends on the perceived signal and nature of the defense response, lead to microbe- or pathogen-associated molecular patterns or damage-associated molecular patterns. The turnover of associated secondary metabolite such as glucosinolate is a suggestion of their roles in key interactions. For instance, the effector-triggered hypersensitive response (ET-HR) mechanism, which depends on indole and aliphatic glucosinolates, or their by-products have been implicated in delayed programmed cell death upon Pseudomonas syringae and Hyaloperonospora arabidopsidis inoculation in aliphatic glucosinolate-deficient myb28 and myb29 plants. These findings confirm that glucosinolates can be involved in ET-HR and ROS pathways.