Genomic and Molecular Outlook of Host-pathogen Interaction and Resistance Strategies against White Rust in Mustard (Brassica juncea L.)

Abstract

White rust, caused by the oomycete pathogen Albugo candida, poses a significant threat to mustard cultivation, leading to reduced yields and compromised oilseed quality. This study explores the genomic and molecular mechanisms underlying the host-pathogen interaction in B. juncea and outlines resistance strategies to counter white rust. While it is the predominant oilseed Brassica species in India, it is cultivated on a smaller scale in China and Australia. Due to its drought-hardy nature, B. juncea is being bred for canola-quality traits to expand its cultivation into lower rainfall regions. Research has demonstrated that resistance to white rust in B. juncea is regulated by a single dominant gene, and numerous lines, such as 'Bio-YSR', 'BEC-144', and 'JM-1', exhibit this trait. Comparative proteomic studies identified 19 proteins with significant expression changes between resistant and susceptible varieties. One key protein, PR-5, a thaumatin-like protein, has been linked to the resistance mechanism. Recent advances in genomic research, including the use of AFLPs, intron polymorphic markers, and SSRs, have enabled breeders to track and validate resistance traits. Enrichment of NLR repertoire, over-expression of R genes, silencing of avirulent and disease susceptibility genes through RNA interference and CRSPR-Cas are technologies which have been successfully applied against pathogen-resistance mechanism. These findings pave the way for genetic-based approaches to develop white rust-resistant B. juncea cultivars, providing a sustainable strategy to protect oilseed production in diverse climatic conditions. This study's insights contribute to a deeper understanding of host-pathogen interactions and offer promising solutions to mitigate the impact of white rust on mustard crops.