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Background Plasmodiophora brassicae is the causal agent of clubroot disease of cruciferous plants and one of the biggest threats to the rapeseed (Brassica napus) and brassica vegetable industry worldwide. Disease symptoms In the advanced stages of clubroot disease wilting, stunting, yellowing, and redness are visible in the shoots. However, the typical symptoms of the disease are the presence of club‐shaped galls in the roots of susceptible hosts that block the absorption of water and nutrients. Host range Members of the family Brassicaceae are the primary host of the pathogen, although some members of the family, such as Bunias orientalis, Coronopus squamatus, and Raphanus sativus, have been identified as being consistently resistant to P. brassicae isolates with variable virulence profile. Taxonomy Class: Phytomyxea; Order: Plasmodiophorales; Family: Plasmodiophoraceae; Genus: Plasmodiophora; Species: Plasmodiophora brassicae (Woronin, 1877). Distribution Clubroot disease is spread worldwide, with reports from all continents except Antarctica. To date, clubroot disease has been reported in more than 80 countries. Pathotyping Based on its virulence on different hosts, P. brassicae is classified into pathotypes or races. Five main pathotyping systems have been developed to understand the relationship between P. brassicae and its hosts. Nowadays, the Canadian clubroot differential is extensively used in Canada and has so far identified 36 different pathotypes based on the response of a set of 13 hosts. Effectors and resistance After the identification and characterization of the clubroot pathogen SABATH‐type methyltransferase PbBSMT, several other effectors have been characterized. However, no avirulence gene is known, hindering the functional characterization of the five intercellular nucleotide‐binding (NB) site leucine‐rich‐repeat (LRR) receptors (NLRs) clubroot resistance genes validated to date. Important Link Canola Council of Canada is constantly updating information about clubroot and P. brassicae as part of their Canola Encyclopedia: https://www.canolacouncil.org/canola‐encyclopedia/diseases/clubroot/. Phytosanitary categorization PLADBR: EPPO A2 list; Annex designation 9E. The clubroot pathogen wants to conquer the world, and how better than through social media. This Plasmodiophora brassicae profile highlights how the growers are in a constant fight with this devastating pathogen. Art by C.‐É. Brochu.

Background The induction of alcohol fermentation in roots is a plant adaptive response to flooding stress and oxygen deprivation. Available transcriptomic data suggest that fermentation-related genes are also frequently induced in roots infected with gall forming pathogens, but the biological significance of this induction is unclear. In this study, we addressed the role of hypoxia responses in Arabidopsis roots during infection by the clubroot agent Plasmodiophora brassicae . Results The hypoxia-related gene markers PYRUVATE DECARBOXYLASE 1 ( PDC1) , PYRUVATE DECARBOXYLASE 2 ( PDC2) and ALCOHOL DEHYDROGENASE 1 ( ADH1) were induced during secondary infection by two isolates of P. brassicae , eH and e2. PDC2 was highly induced as soon as 7 days post inoculation (dpi), i.e., before the development of gall symptoms, and GUS staining revealed that ADH1 induction was localised in infected cortical cells of root galls at 21 dpi. Clubroot symptoms were significantly milder in the pdc1 and pdc2 mutants compared with Col-0, but a null T-DNA insertional mutation of ADH1 did not affect clubroot susceptibility. The Arg/N-end rule pathway of ubiquitin-mediated proteolysis controls oxygen sensing in plants. Mutants of components of this pathway, ate1 ate2 and prt6 , that both exhibit constitutive hypoxia responses, showed enhanced clubroot symptoms. In contrast, gall development was reduced in quintuple and sextuple mutants where the activity of all oxygen-sensing Group VII Ethylene Response Factor transcription factors (ERFVIIs) is absent ( erfVII and prt6 erfVII ). Conclusions Our data demonstrate that the induction of PDC1 and PDC2 during the secondary infection of roots by P. brassicae contributes positively to clubroot development, and that this is controlled by oxygen-sensing through ERFVIIs. The absence of any major role of ADH1 in symptom development may also suggest that PDC activity could contribute to the formation of galls through the activation of a PDH bypass.

Background Plant roots are complex, three-dimensional structures that play a central role in anchorage, water and nutrient acquisition, storage and interaction with rhizosphere microbes. Studying the development of the plant root system architecture is inherently difficult as soil is not a transparent medium. Results This study uses electrical impedance tomography (EIT) to visualise oilseed rape root development in horticultural compost. The development of healthy, control plants and those infected with the gall-forming pathogen, Plasmodiophora brassicae —the causative agent of clubroot disease—were compared. EIT measurements were used to quantify the development of the root system and distinguish between control and infected plants at the onset of gall formation, approximately 20 days after inoculation. Although clear and stark differences between healthy and infected plants were obtained by careful (and hence laborious) packing of the growth medium in layers within the pots; clubroot identification is still possible without a laborious vessel filling protocol. Conclusions These results demonstrate the utility of EIT as a low-cost, non-invasive, non-destructive method for characterising root system architecture and plant-pathogen interactions in opaque growth media. As such it offers advantages over other root characterisation techniques and has the potential to act as a low-cost tool for plant phenotyping.

Clubroot disease is a soil-borne disease caused by Plasmodiophora brassicae. It occurs in cruciferous crops exclusively, and causes serious damage to the economic value of cruciferous crops worldwide. Although different measures have been taken to prevent the spread of clubroot disease, the most fundamental and effective way is to explore and use disease-resistance genes to breed resistant varieties. However, the resistance level of plant hosts is influenced both by environment and pathogen race. In this work, we described clubroot disease in terms of discovery and current distribution, life cycle, and race identification systems; in particular, we summarized recent progress on clubroot control methods and breeding practices for resistant cultivars. With the knowledge of these identified resistance loci and R genes, we discussed feasible strategies for disease-resistance breeding in the future.

Clubroot, caused by Plasmodiophora brassicae , is an important disease of Brassica crops worldwide. F 1 progeny from the Brassica rapa lines T19 (resistant) × ACDC (susceptible) were backcrossed with ACDC, then self-pollinated to produce BC 1 S 1 lines, From genotyping-by-sequencing (GBS) of the parental lines and BC 1 plants, about 1.32 M sequences from T19 were aligned into the reference genome of B . rapa with 0.4-fold coverage, and 1.77 M sequences with 0.5-fold coverage in ACDC. The number of aligned short reads per plant in the BC 1 ranged from 0.07 to 1.41 M sequences with 0.1-fold coverage. A total of 1584 high quality SNP loci were obtained, distributed on 10 chromosomes. A single co-localized QTL, designated as Rcr4 on chromosome A03, conferred resistance to pathotypes 2, 3, 5, 6 and 8. The peak was at SNP locus A03_23710236, where LOD values were 30.3 to 38.8, with phenotypic variation explained (PVE) of 85–95%. Two QTLs for resistance to a novel P . brassicae pathotype 5x, designated Rcr8 on chromosome A02 and Rcr9 on A08, were detected with 15.0 LOD and 15.8 LOD, and PVE of 36% and 39%, respectively. Bulked segregant analysis was performed to examine TIR-NBS-LRR proteins in the regions harboring the QTL.

The rapid spread of clubroot disease, which is caused by , threatens Brassicaceae crop production worldwide. Breeding plants that have broad-spectrum disease resistance is one of the best ways to prevent clubroot. In the present study, eight Chinese cabbage germplasms were screened using published clubroot-resistant (CR) loci-/gene-linked markers. A CR gene Crr3 potential carrier \"85-74\" was detected which linked to marker BRSTS61; however, \"85-74\" shows different responses to local pathogens \"LAB-19,\" \"LNND-2,\" and \"LAB-10\" from \"CR-73\" which harbors Crr3. We used a next-generation sequencing-based bulked segregant analysis approach combined with genetic mapping to detect CR genes in an F segregant population generated from a cross between the Chinese cabbage inbred lines \"85-74\" (CR) and \"BJN3-1\" (clubroot susceptible). The \"85-74\" line showed resistance to a local pathogen \"LAB-19\" which was identified as race 4; a genetic analysis revealed that the resistance was conferred by a single dominant gene. The CR gene which we named was mapped to a 60 kb (1 cM) region between markers yau389 and yau376 on chromosome A03. is located upstream of which was confirmed based on the physical positions of linked markers. The identification of linked markers can be applied to marker-assisted selection in the breeding of new CR cultivars of Chinese cabbage and other crops.

Two cabbage ( Brassica oleracea ) cultivars ‘Tekila’ and ‘Kilaherb’ were identified as resistant to several pathotypes of Plasmodiophora brassicae . In this study, we identified a clubroot resistance gene ( Rcr7 ) in ‘Tekila’ for resistance to pathotype 3 of P. brassicae from a segregating population derived from ‘Tekila’ crossed with the susceptible line T010000DH3. Genetic mapping was performed by identifying the percentage of polymorphic variants (PPV), a new method proposed in this study, through bulked segregant RNA sequencing. Chromosome C7 carried the highest PPV (42%) compared to the 30–34% in the remaining chromosomes. A peak with PPV (56–73%) was found within the physical interval 41–44 Mb, which indicated that Rcr7 might be located in this region. Kompetitive Allele-Specific PCR was used to confirm the association of Rcr7 with SNPs in the region. Rcr7 was flanked by two SNP markers and co-segregated with three SNP markers in the segregating population of 465 plants. Seven genes encoding TIR-NBS-LRR disease resistance proteins were identified in the target region, but only two genes, Bo7g108760 and Bo7g109000 , were expressed. Resistance to pathotype 5X was also mapped to the same region as Rcr7 . B. oleracea lines including ‘Kilaherb’ were tested with five SNP markers for Rcr7 and for resistance to pathotype 3; 11 of 25 lines were resistant, but ‘Kilaherb’ was the only line that carried the SNP alleles associated with Rcr7 . The presence of Rcr7 in ‘Kilaherb’ for resistance to both pathotypes 3 and 5X was confirmed through linkage analysis.

Clubroot, caused by Plasmodiophora brassicae, is an important soilborne disease of canola (Brassica napus) in Alberta, Canada. Genetic resistance is the most effective clubroot management tool, and resistant cultivars are grown extensively in affected regions. In 2013, relatively severe symptoms of clubroot were observed in some fields of resistant canola. In greenhouse tests, four populations of P. brassicae from two of these fields caused significantly increased levels of clubroot on the cultivars from which they had been first recovered; these included three populations (L-G1, L-G2 and L-G3) recovered from the cultivar ‘L135C’, and one population (D-G3) recovered from ‘D3152’. Further testing showed that L-G1, L-G2 and L-G3 were highly virulent on a suite of six resistant canola cultivars (‘45H29’, ‘D3152’, ‘74–47CR’, ‘1960’, ‘L135C’ and ‘6056CR’) representing a cross-section of products available in Canada, while a seventh cultivar (‘9558c’) was moderately resistant to moderately susceptible. Bioassays of field soil with a dozen clubroot-resistant host genotypes confirmed that in most cases, resistance was no longer effective. Host responses to the population D-G3 were more variable, with most cultivars developing intermediate levels of disease. All four P. brassicae populations were classified as pathotypes 5, P₃ and 16/6/8 on the differentials of Williams, Somé et al., and the European Clubroot Differential set. The pathotype classifications, however, do not reflect the increased virulence of these populations on clubroot-resistant canola. The identification of new virulence phenotypes of P. brassicae capable of overcoming genetic resistance underscores the need for increased stewardship of resistance sources.

Plant disease resistance is often under quantitative genetic control. Thus, in a given interaction, plant cellular responses to infection are influenced by resistance or susceptibility alleles at different loci. In this study, a genetic linkage analysis was used to address the complexity of the metabolic responses of Brassica napus roots to infection by Plasmodiophora brassicae. Metabolome profiling and pathogen quantification in a segregating progeny allowed a comparative mapping of quantitative trait loci (QTLs) involved in resistance and in metabolic adjustments. Distinct metabolic modules were associated with each resistance QTL, suggesting the involvement of different underlying cellular mechanisms. This approach highlighted the possible role of gluconasturtiin and two unknown metabolites in the resistance conferred by two QTLs on chromosomes C03 and C09, respectively. Only two susceptibility biomarkers (glycine and glutathione) were simultaneously linked to the three main resistance QTLs, suggesting the central role of these compounds in the interaction. By contrast, several genotype-specific metabolic responses to infection were genetically unconnected to resistance or susceptibility. Likewise, variations of root sugar profiles, which might have influenced pathogen nutrition, were not found to be related to resistance QTLs. This work illustrates how genetic metabolomics can help to understand plant stress responses and their possible links with disease.

Marine representatives of Phytomyxea (SAR: Rhizaria: Endomyxa), a peculiar class of obligate endobiotic parasites, are a greatly understudied ecological group of protists infecting many algal, diatom, and seagrass species. Very little is known about the actual diversity, ecology, and pathogenic potential of these organisms and their taxonomic treatment in many cases follows outdated morphotaxonomic concepts. Here we focused on resolving the phylogenetic relations of the phytomyxean parasites of the widespread seagrass genus Halophila. We report the first finding of Plasmodiophora halophilae, the parasite of ovate-leaf Halophila species, after more than 100 years since its original description in 1913. We provide additional information on its anatomy, morphology, distribution, and host range, together with a phylogenetic evidence that it is congeneric with the recently rediscovered species infecting the invasive seagrass Halophila stipulacea in the Mediterranean Sea. Despite the previously hypothesized affiliation of the latter to Tetramyxa, our phylogenetic analyses of the 18S rRNA gene place Tetramyxa parasitica (a parasite of brackish water phanerogams and the type species of the genus) in the freshwater/terrestrial phytomyxean order Plasmodiophorida and reveal that phytomyxids associated with Halophila spp. form a separate deep-branching clade within the class proposed here as Marinomyxa gen. nov. We further argue that M. marina infecting H. stipulacea is most likely a speciesspecific parasite and implies their comigration through the Suez Canal.