Genetic and epigenetic mechanisms underpinning biotic stress resilience of Brassica vegetables

Breeding for disease-resistant varieties is a sustainable solution to reduce substantial production losses caused by pathogenic infestations in Brassica vegetables, bypassing environmentally risky disease management practices. Host-resistant genetic mechanisms aid breeders to identify resistance loci and linked markers for the clubroot, Fusarium yellows, downy mildew, black rot, stem rot, soft rot, white rust, and turnip mosaic virus diseases in Brassica vegetables. Introgression of the resistance (R) genes by marker-assisted selection (MAS) breeding strategies allow the development of disease-resilient varieties. Brassica rapa clubroot-resistant genes (CRa, CRc, CRd, CRk, and Crr5) have been introgressed into Chinese cabbage, while CR genes (CRa, CRb, CRc, Crr1, Crr2, and Crr3) from B. rapa were also introgressed into B. oleracea. Beyond MAS, R genes can be precisely engineered by CRISPR-based technologies into precise and durable resistant varieties. The involvement of DNA methylation and histone modifications epigenetically regulate resistance mechanisms, often via ethylene/salicylic acid/jasmonic acid signaling pathways. DNA methylation mediates systemic acquired resistance by the differential expression of genes such as JAZ1, PR3, and NDR1. Future progress will depend on identifying epiQTLs and epi-markers linked to R genes. Epigenetic insights with genetic knowledge will facilitate breeding of biotic stress-resilient Brassica vegetables. This review synthesizes current molecular understanding of biotic stressors and provides future directions for disease resistance breeding of Brassica vegetable plants.