Clubroot, caused by Plasmodiophora brassicae Wor., is an important soilborne disease of canola (Brassica napus L.) in Canada that is managed mainly by planting clubroot-resistant (CR) cultivars. Populations of P. brassicae representing 106 fields in Alberta were obtained from galled roots of CR canola plants collected in 2014–2016 and characterized for virulence on seven CR canola cultivars. Sixty-one of these populations could overcome resistance in at least one CR cultivar and were evaluated further by inoculation on 13 Brassica hosts termed the Canadian Clubroot Differential (CCD) Set. The CCD Set included the differentials of Williams and Somé et al., selected hosts of the European Clubroot Differential Set, and the B. napus cultivars ‘Brutor’, ‘Mendel’, ‘Westar’ and ‘45H29’. Each unique virulence pattern on the CCD Set represented a distinct pathotype and was identified with a letter. Five reference isolates, obtained prior to the introduction of CR canola, also were assessed. A total of 17 pathotypes were detected using the CCD Set, compared with five pathotypes using the system of Williams and two with the system of Somé et al., suggesting that the CCD Set has a greater differentiating capacity. Pathotype A, a variant of pathotype 3 (as per Williams) which is able to overcome the resistance in CR B. napus, was predominant. The original pathotype 3, which is avirulent on CR canola, was classified as CCD pathotype H. An integrated strategy, combining other tools in addition to resistance, will be needed for the sustainable management of clubroot.

Clubroot resistance derived from the oilseed rape/canola Brassica napus ‘Mendel’ has been overcome in some fields in Alberta, Canada, by the emergence of ‘new’ strains of the protist Plasmodiophora brassicae . Resistance to the pathogen was assessed in 112 doubled haploid ( DH ) lines, derived from B. rapa subsp. rapifera (European clubroot differential ( ECD ) 04). The lines were evaluated against five single‐spore isolates representing the ‘old’ pathotypes 2, 3, 5, 6 and 8, and 15 field populations representing new strains of P. brassicae . The disease severity index ( ID %) data revealed that none of the DH lines were resistant or moderately resistant to the new pathotype 5X (field populations L‐G1, L‐G2, L‐G3) and D‐G3, while 3–42% were resistant or moderately resistant to the other 11 new strains. Using the mean ID induced by the old pathotype 3 (approx. 13.5%) as the baseline, clubroot severity increased by 300–600% when inoculated with the new pathotypes. A significant finding of this study was the fact that ECD 04 showed absolute resistance to all of the old and new P. brassicae strains while the B. napus ‘Mendel’, although resistant to all of the old pathotypes, was resistant to only about 50% of the new strains. Similarly, all of the selected clubroot‐resistant commercial canola cultivars evaluated in this study were susceptible to 87% of the new P. brassicae strains. The molecular data revealed that the breakdown of clubroot resistance in Mendel and the canola cultivars was in part due to the non‐inheritance of the Crr1 gene on the A08 chromosome from ECD 04.

Rutabaga [Brassica napus ssp. napobrassica (L.) Hanelt] is reported to be an excellent source of clubroot (Plasmodiophora brassicae) resistance genes. In this study, 124 rutabaga accessions from the Nordic countries (Norway, Sweden, Finland, Denmark, and Iceland) were evaluated for their reaction to five single-spore isolates representing P. brassicae pathotypes 2F, 3H, 5I, 6M, and 8N and 12 field isolates representing pathotypes 2B, 3A, 3O, 5C, 5G, 5K, 5L, 5X (two isolates, L-G2 and L-G3), 8E, 8J, and 8P. The accessions were also genotyped using a 15K Brassica SNP array and 60 PCR-based primers linked to previously identified clubroot resistance genes. Six thousand eight hundred sixty-one SNP markers were retained after filtering with TASSEL 5.0, and used to evaluate four general linear models (GLM) and four mixed linear models (MLM). The PCA + K and Q + K MLM models gave the minimal deviance of the observed from the expected distribution in quantile-quantile plots, and hence were used for SNP-clubroot association analyses. In addition, 108 alleles derived from the PCR-based markers and the phenotypic data were analyzed with the PCA + K model. Forty-five SNPs and four PCR-based markers were identified to be associated strongly with resistance to isolates representing 13 pathotypes (2F, 3H, 5I, 6M, 8N, 2B, 3A, 3O, 5C, 5G, 5K, 5L, and 8P). These markers revealed the top and bottom segments of rutabaga chromosome A03 and the middle segment of chromosome A08 as genomic hotspots associated with resistance to the different P. brassicae pathotypes.