Clubroot disease, caused by Plasmodiophora brassicae, affects Brassica oilseed and vegetable production worldwide. This review is focused on various aspects of clubroot disease and its management, including understanding the pathogen and resistance in the host plants. Advances in genetics, molecular biology techniques, and omics research have helped to identify several major loci, QTL, and genes from the Brassica genomes involved in the control of clubroot resistance. Transcriptomic studies have helped to extend our understanding of the mechanism of infection by the pathogen and the molecular basis of resistance/susceptibility in the host plants. A comprehensive understanding of the clubroot disease and host resistance would allow developing a better strategy by integrating the genetic resistance with cultural practices to manage this disease from a long-term perspective.

Clubroot resistance in spring canola has been introgressed from different Brassica sources; however, molecular mechanism underlying this resistance, especially the involvement of long non-coding RNAs (lncRNAs), is yet to be understood. We identified 464 differentially expressed (DE) lncRNAs from the roots of clubroot-resistant canola, carrying resistance on chromosome BnaA03, and susceptible canola lines challenged with Plasmodiophora brassicae pathotype 3. Pathway enrichment analysis showed that most of the target genes regulated by these DE lncRNAs belonged to plant–pathogen interaction and hormone signaling, as well as primary and secondary metabolic pathways. Comparative analysis of these lncRNAs with 530 previously reported DE lncRNAs, identified using resistance located on BnaA08, detected 12 lncRNAs that showed a similar trend of upregulation in both types of resistant lines; these lncRNAs probably play a fundamental role in clubroot resistance. We identified SSR markers within 196 DE lncRNAs. Genotyping of two DH populations carrying resistance on BnaA03 identified a marker capable of detecting the resistance in 98% of the DH lines. To our knowledge, this is the first report of the identification of SSRs within lncRNAs responsive to P. brassicae infection, demonstrating the potential use of lncRNAs in the breeding of Brassica crops.

Understanding the intricate molecular interplay between Brassica hosts and the pathogen Plasmodiophora brassicae, causative agent of clubroot disease, is pivotal for devising effective resistance to this disease in Brassica crops. While existing transcriptomic studies have elucidated the host responses to pathogen infection, a comprehensive analysis employing near-isogenic lines (NILs) remains imperative for better understanding of the resistance mechanisms. In this study, we conducted a comparative transcriptome profiling utilizing clubroot-susceptible (CS-NILs) and clubroot-resistant (CR-NILs) near-isogenic Brassica napus lines, carrying the clubroot resistance of turnip (B. rapa var. rapifera), at 7 and 14 days after inoculation. We observed the upregulation of the genes governing phytohormone signaling, receptor kinases, transcription factors, calcium fluxes, and glucosinolate metabolism in the CR-NILs. In addition, the novel differentially expressed genes (DEGs) pertaining to jasmonic acid, calcium signaling, receptor kinases, and glucosinolate biosynthesis were also observed to be differentially expressed. Based on our results, we propose a comprehensive model delineating the molecular events potentially contributing to clubroot resistance in B. napus CR-NILs. Our findings have contributed to an enhanced understanding of the potential mechanisms involved in clubroot resistance which may have utility in targeted breeding initiatives to mitigate the threat of clubroot disease in Brassica crops including canola.