QTL Mapping and Inheritance of Clubroot Resistance Genes Derived From subsp. (ECD 02) Reveals Resistance Loci and Distorted Segregation Ratios in Two Populations of Different Crosses.

In this study, subsp. (ECD 02) which exhibits broad-spectrum resistance to many Canadian isolates was crossed with two clubroot-susceptible accessions to produce two populations. The plants were screened against pathotypes 3H, 5X, and 5G. The Chi-square goodness of fit test showed that the vast majority (≈75%) of the crosses that produced the populations showed segregation ratios of 9R:7S, 7R:9S, 13R:3S, 3R:13S, 5R:11S, 11R:5S, and 1R:15S. These were modifications of the 15R:1S ratio expected for the inheritance of two dominant major clubroot resistance (CR) genes from ECD 02. The distorted segregation ratios suggest that the two resistance genes are on different chromosomes and that two genes interact in an epistatic manner to confer resistance. Genotyping was conducted with 144 PCR-based markers in the two populations. Linkage and QTL analysis with the polymorphic markers identified two QTLs on chromosome A03 to be associated with resistance to pathotypes 5X and 5G in Popl#1 while only the second QTL on chromosome A03 was associated with resistance to pathotypes 5X and 5G in Popl#2. The QTLs clustered in genomic regions on the A03 chromosome of where the / gene(s) are mapped. In addition, the gene on the A08 chromosome of was detected in the two populations. Therefore, the phenotypic and molecular data confirm the existence of two CR genes in ECD 02. This is the first study that shows that major dominant genes in interact in a non-additive manner to confer resistance to different pathotypes. This study provides knowledge on the inheritance and type of gene action for clubroot resistance derived from subsp. (ECD 02). The results indicated that duplicate recessive and recessive suppression epistatic interactions, digenic additivity and complementary gene action between the / gene(s) on the A03 and the gene on the A08 chromosome of controlled clubroot resistance to pathotypes 3H, 5X and 5G.