Genetic analysis of clubroot resistance in Brassica crops

Clubroot disease is caused by an obligate parasite, Plasmodiophora brassicae, and is one of the most serious diseases of Brassica crops worldwide. The pathogen is a eukaryote, and is a member of Plasmodiophorales. Recent phylogenic studies did not reveal its close relationship to fungi, but suggest a classification in Protozoa or Protoctista. The infection is thought to occur through two phases. The pathogen induces massive clubs on root, and prevents host growth. A number of clubroot resistance (CR) Chinese cabbage (Brassica rapa) cultivars have been bred using European turnips as sources of CR genes. Field populations of the pathogen have a wide variation of virulence, which causes the infection of CR Chinese cabbage cultivars. The CR gene of B. rapa is extensively studied with the aid of molecular markers. At least four independent loci are identified and mapped. They are all derived from European turnips. Crr1, and Crr2 are derived from Siloga and mapped in linkage groups R8 and R6, respectively. Crr3 from Milan White, and CRb from Gelria R are both mapped in R3. The molecular markers linked to Crr1, Crr2 and CRb showed homology to the central part of the long arm of chromosome 4 of Arabidopsis thaliana. These findings suggest that these CR genes are derived from the same region of the ancestral genome. In contrast, Crr3 is thought to have different origin, since its linkage markers showed homology to chromosome 3 of A. thaliana. Although another CR gene CRa is reported, the relationship between above mentioned four CR loci and CRa is not yet clarified. Genetic studies on CR genes in B. oleracea revealed a polygenic nature of the trait in this species and also suggest the presence of one CR gene having large effect. However, correspondence among the CR genes reported in these studies is not clarified because of the lack of information on base sequence of the linkage markers in this species. Strategies for breeding of more resistant Chinese cabbage cultivars to overcome the variation on virulence of field populations of the pathogen are presented.