Clubroot disease caused by Plasmodiophora brassicae Woronin is a concern to the canola (Brassica napus L.) growers in Canada. A crop management strategy that includes deployment of genetic resistance and appropriate cultural practices is needed for long-term management of this disease. Resistance to the P. brassicae pathotypes present in Canada has been found in the primary and secondary gene pools of spring B. napus canola. Some of these sources, such as winter canola ‘Mendel’, rutabaga and Pak Choi (Brassica rapa L.) ‘Flower Nabana’, were used in genetic studies and breeding for the development of clubroot-resistant canola cultivars. A dominant gene in ‘Mendel’ and ‘Flower Nabana’ was found to confer resistance to P. brassicae pathotype 3, while a simple or a complex genetic control of resistance was found in rutabaga. The clubroot resistance (CR) gene in ‘Flower Nabana’ was mapped to chromosome A3, and molecular markers linked to the CR gene were identified for use in marker-assisted breeding (MAB). Using the CR genes from ‘Mendel’ and rutabaga, several clubroot-resistant spring canola lines were developed. Often the CR genes of ‘Mendel’ and rutabaga conferring resistance to pathotype 3 also conferred resistance to other pathotypes of P. brassicae found in Canada, including pathotypes 5, 6 and 8. The CR gene of ‘Flower Nabana’ was introgressed into B. napus and B. rapa canola through MAB. Since single-gene controlled resistance can be eroded, other strategies such as pyramiding different CR genes into B. napus canola should be considered for durable resistance.

Clubroot disease, caused by Plasmodiophora brassicae, is a threat to the production of Brassica crops including oilseed B. napus. In Canada, several pathotypes of this pathogen, such as pathotypes 2, 3, 5, 6, and 8, were identified, and resistance to these pathotypes was found in a rutabaga (B. napus var. napobrassica) genotype. In this paper, we report the genetic basis and molecular mapping of this resistance by use of F₂, backcross (BC₁), and doubled haploid (DH) populations generated from crossing of this rutabaga line to a susceptible spring B. napus canola line. The F₁, F₂, and BC₁ populations were evaluated for resistance to pathotype 3, and the DH population was evaluated for resistance to pathotypes 2, 3, 5, 6, and 8. A 3:1 segregation in F₂ and a 1:1 segregation in BC₁ were found for resistance to pathotype 3, and a 1:1 segregation was found in the DH population for resistance to all pathotypes. Molecular mapping by using the DH population identified a genomic region on chromosome A8 carrying resistance to all five pathotypes. This suggests that a single gene or a cluster of genes, located in this genomic region, is involved in the control of resistance to these pathotypes.