Drought reduces Ascochyta rabiei infection in chickpea through proline/P5C/mitochondrial-ROS mediated fungal suppression

Co-occurring abiotic and biotic stresses can have negative or positive interactions with plants. Previously, our field study showed reduced incidence of Ascochyta blight in chickpea under drought conditions. Here, we investigated chickpea’s molecular responses to Ascochyta rabiei under drought, pathogen and combined stress using transcriptomics, gene expression, and amino acid profiling, identifying proline dehydrogenase (CaProDH2) as a key regulator of resistance under combined stress. MiRNA-induced silencing (MIGS) of CaProDH2 reduced the expression of pathogen stress-responsive genes and lowered mitochondrial P5C and superoxide levels under combined stress. In contrast, CaProDH2 overexpression restricted fungal colonization and reduced in-planta fungal load. Co-transcriptome analysis of wild-type plants under combined stress showed suppression of fungal growth- and virulence-associated genes. Here we show that CaProDH2 mediates the catabolism of drought-induced proline, thereby triggering a defense response involving mitochondrial ROS, which likely induces cell death in A. rabiei . Our findings highlight how co-occurring stresses can interact positively, linking drought-induced metabolic changes to fungal resistance through the proline/P5C pathway.