Effector molecules and pathogenicity-associated gene expression in Ascochyta rabiei

The necrotrophic fungus Ascochyta rabiei poses a significant threat to chickpea cultivation worldwide, leading to severe yield losses and quality reduction. Understanding the molecular mechanisms behind the pathogenicity of A. rabiei is essential for developing effective management strategies. This study employed transcriptomic analyses to compare the gene expression profiles among two A. rabiei isolates with differing pathogenicity levels (highly pathogenic AR0231 and low pathogenic AR0225) during interaction of PBA HatTrick chickpea genotype at the early podding stage. PBA HatTrick is classified as moderately susceptible to A. rabiei based on field trial ratings from the GRDC National Variety Trials. Like most cultivated chickpea varieties, its resistance to A. rabiei is generally considered polygenic and quantitative in nature, with no major resistance gene identified to date. A total of 105 differentially expressed genes (DEGs) were identified, including 57 upregulated and 48 downregulated in AR0231. Notably, effector-related genes were prominent among the upregulated DEGs, including EKO05_0002468, a homolog of the CoNIS1 effector gene that suppresses plant immunity, and EKO05_0010552, a homolog of PsGIP2/PsGIP1 encoding a glucanase inhibitor that protects fungal cell walls from host enzymes. Additionally, EKO05_0001368, homologous to PesCDA/VdPDA1, encodes a chitin-binding effector linked to immune evasion. Downregulated DEGs included EKO05_0006947, a LysM-domain effector homolog implicated in masking fungal chitin from host detection. These findings provide new insights into the molecular mechanisms employed by A. rabiei during infection of mature chickpea tissue and highlight candidate genes for future research on improving chickpea resistance to Ascochyta blight.