Transcriptome Analysis of the Necrotrophic Pathogen Alternaria brassicae Reveals Insights into Its Pathogenesis in...

Alternaria blight or leaf spot caused by Alternaria brassicae has an enormous economic impact on the Brassica crops grown worldwide. Although the genome of A. brassicae has been sequenced, little is known about the genes that play a role during the infection of the host species. In this study, the transcriptome expression profile of A. brassicae during growth and infection was determined. Differential expression analysis revealed that 4,430 genes were differentially expressed during infection. Weighted gene coexpression network analysis helped identify 10 modules, which were highly correlated with growth and infection. Subsequent gene ontology (GO) enrichment analysis of the modules highlighted the involvement of biological processes such as toxin metabolism, ribosome biogenesis, polysaccharide catabolism, copper ion transport, and vesicular trafficking during infection. Additionally, 200 carbohydrate-active enzymes (CAZymes) and 80 potential effectors were significantly upregulated during infection. Furthermore, 18 secondary metabolite gene clusters were also differentially expressed during infection. The clusters responsible for the production of destruxin B, brassicicene C, and HC-toxin were significantly upregulated during infection. Collectively, these results provide an overview of the critical pathways underlying the pathogenesis of A. brassicae and highlight the distinct gene networks that are temporally regulated. The study thus provides novel insights into the transcriptional plasticity of a necrotrophic pathogen during infection of its host. Additionally, the in planta expression evidence for many potential effectors provides a theoretical basis for further investigations into the effector biology of necrotrophic pathogens such as A. brassicae. IMPORTANCE Alternaria brassicae is a necrotrophic pathogen that can infect almost all members of the Brassicaceae family. A. brassicae causes extensive yield losses in oilseed mustard and has practically restricted the cultivation of oilseed brassicas in regions with cool and foggy climatic conditions (foothills and mountainous terrains) where the severity of the pathogen is the highest. In this study, I identified the differentially expressed genes associated with the pathogenicity of A. brassicae through transcriptome sequencing. Also, I have been able to delineate pathways that are active during the early and late stages of infection. Consequently, this study has provided crucial insights into the molecular mechanisms underlying the pathogenesis of A. brassicae, an important necrotrophic pathogen.