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.

The protist Plasmodiophora brassicae is a soil-borne pathogen of cruciferous species and the causal agent of clubroot disease of Brassicas including agriculturally important crops such as canola/rapeseed (Brassica napus). P. brassicae has remained an enigmatic plant pathogen and is a rare example of an obligate biotroph that resides entirely inside the host plant cell. The pathogen is the cause of severe yield losses and can render infested fields unsuitable for Brassica crop growth due to the persistence of resting spores in the soil for up to 20 years. To provide insight into the biology of the pathogen and its interaction with its primary host B. napus, we produced a draft genome of P. brassicae pathotypes 3 and 6 (Pb3 and Pb6) that differ in their host range. Pb3 is highly virulent on B. napus (but also infects other Brassica species) while Pb6 infects only vegetable Brassica crops. Both the Pb3 and Pb6 genomes are highly compact, each with a total size of 24.2 Mb, and contain less than 2 % repetitive DNA. Clustering of genome-wide single nucleotide polymorphisms (SNP) of Pb3, Pb6 and three additional re-sequenced pathotypes (Pb2, Pb5 and Pb8) shows a high degree of correlation of cluster grouping with host range. The Pb3 genome features significant reduction of intergenic space with multiple examples of overlapping untranslated regions (UTRs). Dependency on the host for essential nutrients is evident from the loss of genes for the biosynthesis of thiamine and some amino acids and the presence of a wide range of transport proteins, including some unique to P. brassicae. The annotated genes of Pb3 include those with a potential role in the regulation of the plant growth hormones cytokinin and auxin. The expression profile of Pb3 genes, including putative effectors, during infection and their potential role in manipulation of host defence is discussed. The P. brassicae genome sequence reveals a compact genome, a dependency of the pathogen on its host for some essential nutrients and a potential role in the regulation of host plant cytokinin and auxin. Genome annotation supported by RNA sequencing reveals significant reduction in intergenic space which, in addition to low repeat content, has likely contributed to the P. brassicae compact genome.

Clubroot, caused by the obligate parasite Plasmodiophora brassicae, is an important soilborne disease of the Brassicaceae. In Canada, clubroot has long been a problem in cruciferous vegetables, but was not reported on the Prairie canola (Brassica napus) crop until 2003, when 12 clubroot-infested fields were identified in central Alberta. Continued surveillance has shown that the disease is spreading, and at least 1064 fields in the province had confirmed clubroot infestations as of 2012. While the outbreak is still mainly confined to central Alberta, isolated clubroot infestations and the presence of viable P. brassicae inoculum have been confirmed in southern Alberta, Saskatchewan and Manitoba. Dissemination of the parasite appears to be predominantly through the movement of infested soil on farm and other machinery, although secondary mechanisms of spread, such as by wind and water erosion and soil contamination of seeds, also have been implicated. Numerous strains of P. brassicae occur in Canada, but pathotype 3 or 16/15/12, as classified on the differentials of Williams or the European Clubroot Differential series, predominates on canola. Given the significant economic value of Canadian canola, the emergence of clubroot on this crop has caused major concern and led to the initiation of a large, coordinated research effort aimed at understanding and managing this disease. This review summarizes the extent and nature of the clubroot outbreak in the Canadian canola crop, 10 years after it began, and provides a context for ongoing research and management efforts.

Genetic resistance is widely used to manage clubroot (Plasmodiophora brassicae) in brassica crops, but new pathotypes have recently been identified on canola (Brassica napus) on the Canadian prairies. Resistance effective against both the most prevalent pathotype (3H, based on the Canadian Clubroot Differential system) and the new pathotypes is needed. BC₁ plants of Brassica rapa from a cross of line 96-6990-2 (clubroot resistance originating from turnip cultivar ‘Waaslander’) and a susceptible doubled-haploid line, ACDC, exhibited a 1:1 segregation for resistance against pathotypes 3H and 5X. A resistance gene designated as Rcr3 was mapped initially based on the percentage of polymorphic variants using bulked segregant RNA sequencing (BSR-Seq) and further mapped using Kompetitive Allele Specific PCR. DNA variants were identified by assembling short reads against a reference genome of B. rapa. Rcr3 was mapped into chromosome A08. It was flanked by single nucleotide polymorphisms (SNP) markers (A90_A08_SNP_M12 and M16) between 10.00 and 10.23 Mb, in an interval of 231.6 Kb. There were 32 genes in the Rcr3 interval. Three genes (Bra020951, Bra020974, and Bra020979) were annotated with disease resistance mechanisms, which are potential candidates for Rcr3. Another resistance gene, designated as Rcr9^wa, for resistance to pathotype 5X was mapped, with the flanking markers (A90_A08_SNP_M28 and M79) between 10.85 and 11.17 Mb using the SNP sites identified through BSR-Seq for Rcr3. There were 44 genes in the Rcr9^wa interval, three of which (Bra020827, Bra020828, Bra020814) were annotated as immune-system-process related genes, which are potential candidates for Rcr9^wa.