What is the impact of the fungus Alternaria brassicae on crops?
Black spot disease of some brassica crops like broccoli, oilseed rape, and cabbage is caused by the fungus Alternaria brassicae. This facultative parasite colonizes susceptible hosts as well as dead plant material causing host-specific toxins. This disease produces a considerable reduction of both yield and seed quality. A. brassicae is the prime causative agent of Alternaria blight disease, which affects most brassica crops globally, causing economic losses with no proven source of transferrable resistance in any of its hosts. In tropical regions, this pathogen is most destructive in the wet season.
The report of Giri suggested that the production of antifungal substance(s) in resistant B. juncea leaves was responsible for reduced infection by Alternaria brassicae. This includes GSLs that affect the differential expression of resistance across different plant species, lines as well as cultivars of the same species or within different tissues of a plant. The antifungal byproducts are not formidable in resistance of these pathogens. However, they remain a key defense system in many brassica plants. GSLs and their hydrolysis products have also been shown previously to have antimicrobial properties. Recently, more specific pathways of this antifungal mechanism were reported by Klein and Sattely. These researchers identified some key enzymes required for the synthesis of the parent phytoalexin of brassica plants called Brassinin from well-studied GSLs. Some of the brassinin-type phytoalexins may be more tightly linked to the biosynthetic pathway of IGSLs. The carbon-sulfur lyase SUR1 processes cysteine–isothiocyanate conjugates, as well as the S-methyltransferase DTCMT that methylates the resulting dithiocarbamate, together completing a pathway to brassinin. Also, the β-glucosidase BABG that is present in Brassica rapa but absent in Arabidopsis was shown by these researchers to act as a myrosinase and may be a determinant of plants that synthesize phytoalexins from IGSLs.