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Clubroot disease is devastating to crop production when susceptible cultivars are planted in infected fields. European turnips are the most resistant sources and their resistance genes have been introduced into other crops such oilseed rape ( L.), Chinese cabbage and other vegetables. The European clubroot differential (ECD) set contains four turnip accessions (ECD1-4). These ECD turnips exhibited high levels of resistance to clubroot when they were tested under controlled environmental conditions with Canadian field isolates. Gene mapping of the clubroot resistance genes in ECD1-4 were performed and three independent dominant resistance loci were identified. Two resistance loci were mapped on chromosome A03 and the third on chromosome A08. Each ECD turnip accession contained two of these three resistance loci. Some resistance loci were homozygous in ECD accessions while others showed heterozygosity based on the segregation of clubroot resistance in 20 BC families derived from ECD1 to 4. Molecular markers were developed linked to each clubroot resistance loci for the resistance gene introgression in different germplasm.

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.

Plasmodiophora brassicae , which is known for its broad genetic diversity for virulence, is the causal agent of clubroot disease of Brassica crops worldwide. Studies on pathotype characterization with four differential hosts according to Williams’ classification system showed the predominance of pathotype 4 in China. However, the genetic variability within pathotype 4 complicates the breeding of durable clubroot-resistant (CR) cultivars. Herein, a Sinitic clubroot differential (SCD) set was developed using a set of eight differential inbred lines of Chinese cabbage with known or novel CR genes. The presence of immense diversity within pathotype 4 of Williams’ system was verified, and 11 pathotypes were characterized using the developed SCD system. The scalability and practicability of the system was further confirmed with a subset of 95 field isolates from different Brassica crops and different regions of China and Korea. Sixteen pathotypes were detected from 132 field isolates, named Pb1 to Pb16, respectively. Among them, Pb1 and Pb4 were prevalent in diverse Brassica crops in the southern and northern regions of China. Pb12, Pb13, Pb14, and Pb16 showed area-specific distribution. The SCD set developed herein will provide important genetic resources for pathogenicity studies of P. brassicae and for CR breeding in Chinese cabbage and other Brassica crops.

Plasmodiophora brassicae , an obligate biotrophic pathogen-causing clubroot disease, can seriously affect Brassica crops worldwide, especially Chinese cabbage. Understanding the transcriptome and metabolome profiling changes during the infection of P. brassicae will provide key insights in understanding the defense mechanism in Brassica crops. In this study, we estimated the phytohormones using targeted metabolome assays and transcriptomic changes using RNA sequencing (RNA-seq) in the roots of resistant (BrT24) and susceptible (Y510-9) plants at 0, 3, 9, and 20 days after inoculation (DAI) with P. brassicae . Differentially expressed genes (DEGs) in resistant vs. susceptible lines across different time points were identified. The weighted gene co-expression network analysis of the DEGs revealed six pathways including “Plant–pathogen interaction” and “Plant hormone signal transduction” and 15 hub genes including pathogenic type III effector avirulence factor gene ( RIN4 ) and auxin-responsive protein ( IAA16 ) to be involved in plants immune response. Inhibition of Indoleacetic acid, cytokinin, jasmonate acid, and salicylic acid contents and changes in related gene expression in R-line may play important roles in regulation of clubroot resistance (CR). Based on the combined metabolome profiling and hormone-related transcriptomic responses, we propose a general model of hormone-mediated defense mechanism. This study definitely enhances our current understanding and paves the way for improving CR in Brassica rapa .

Clubroot, a severe soil‐borne disease caused by Plasmodiophora brassicae, poses a severe threat to global production of Brassicaceae oilseed crops and vegetables. To date, there has been a serious lack of clubroot‐resistant germplasms in Brassica napus (AACC), necessitating the urgent development of novel disease‐resistant germplasm. We present a high‐quality genome assembly of an artificially synthesised allotetraploid Raphanobrassica (RRCC), which exhibits broad‐spectrum immunity to diverse P. brassicae pathotypes. Using a sesquidiploid RACC as a genetic bridge, we developed B. napus‐R. sativus (AACC‐R) monosomic addition lines and mapped a major clubroot resistance (CR) locus on chromosome R5. Comparative genomic analysis identified 30 candidate CR genes in this region. Notably, overexpression of CRR5.5.11, which encodes a receptor‐like protein, via hairy root transformation conferred significant resistance in susceptible B. napus. Evolutionary and functional analyses revealed conserved homologues of CRR5.5.11 in diploid Isatis tinctoria and triploid turnip ECD04. Furthermore, the ECD04 allele CRA3.2.2 also conferred clubroot resistance, indicating that CRR5.5.11 and CRA3.2.2 have originated from the same diploid ancestor. Our study elucidates the genetic and evolutionary basis of clubroot resistance in Raphanobrassica, providing novel germplasm, gene resources and theoretical insights for clubroot‐resistance breeding in rapeseed and other Brassicaceae crops.

Clubroot disease, caused by Plasmodiophora brassicae , is one of the major constraints in rapeseed production. Breeding disease-resistant cultivars is the best way to control this devastating disease. However, breeding reliable resistant germplasm and genes is limited. Inactivation of susceptible genes has been shown to be a new and effective strategy for developing resistant crops. Therefore, we aimed to screen key candidate susceptible genes in this study. Firstly, we established a stable, high-throughput visualization method for identifying gall formation at the early stage of P.brassicae infection. At 14 days post-inoculation (dpi), the earliest time point with a clear record of scorable root swelling, remarkable variations in the speed of gall formation were observed among 85 genotypes. Secondly, genome-wide association studies (GWAS) were performed to identify genes involved in gall development. Three and two consecutive significant peaks were detected at 14 and 21 dpi, respectively. Thirdly, comparative transcriptomic analysis was conducted between 2AF195 and 2AF058 at 7 and 14 dpi; these two materials exhibit contrasting speeds of gall development. Gene clustering analysis revealed two opposite expression patterns at 14 dpi. One pattern comprised 1,383 genes downregulated in 2AF195 but upregulated in 2AF058, which were significantly enriched in 10 KEGG pathways, including Environmental Information Processing and Plant-pathogen interaction, and involved core repressors JAZ8/10 in the jasmonic acid (JA) signaling pathway, as well as nucleotide-binding site (NBS) protein-encoding genes. The opposite pattern consisted of 79 genes upregulated in 2AF195 but downregulated in 2AF058, which were enriched in an additional 10 KEGG pathways, predominantly related to Carbohydrate Metabolism and the Ubiquitin System. These genes were functionally annotated mainly as pectin methylesterases, xyloglucan endotransglucosylase/hydrolases (XTHs), and lignin biosynthesis-related enzymes. These findings demonstrated that distinct regulatory networks exist in different susceptible rapeseed genotypes. Finally, through the combined analysis of haplotype and transcriptome data, we co-localized and identified the candidate gene BnaC08g46100D , a nodulin-related gene belonging to the MtN21 transporter family. These results provide a theoretical basis for developing novel disease-resistant materials by editing the key susceptibility genes involved in root gall formation. The candidate genes identified in this study are the most promising targets for this purpose.

Clubroot disease in canola ( Brassica napus ) continues to spread across the Canadian prairies. Growing resistant cultivars is considered the most economical means of controlling the disease. However, sources of resistance to clubroot in B. napus are very limited. In this study, we conducted interspecific crosses using a B. rapa line (T19) carrying race-specific resistance genes and two B. oleracea lines, ECD11 and JL04, carrying race non-specific QTLs. Employing embryo rescue and conventional breeding methods, we successfully resynthesized a total of eight B. napus lines, with four derived from T19 × ECD11 and four from T19 × JL04. Additionally, four semi-resynthesized lines were developed through crosses with a canola line (DH16516). Testing for resistance to eight significant races of Plasmodiophora brassicae was conducted on seven resynthesized lines and four semi-resynthesized lines. All lines exhibited high resistance to the strains. Confirmation of the presence of clubroot resistance genes/QTLs was performed in the resynthesized lines using SNP markers linked to race-specific genes in T19 and race non-specific QTLs in ECD11. The developed B. napus germplasms containing clubroot resistance are highly valuable for the development of canola cultivars resistant to clubroot.

The narrow genetic base of current (AABB) has limited the genetic improvement of this crop. In this study, we developed novel germplasm by crossing synthetic hexaploid bridge lines (AABBBB and AAAABB) with diploid progenitors  (AA) and (BB), followed by successive selfing and marker-assisted selection. Although the F1 hybrids exhibited wide variation in fertility and morphology, these traits stabilized at levels comparable to current by the F2 and F3 generations. Whole-genome resequencing confirmed that the new-type lines not only constitute a unique genetic group but also show a genomic shift toward the current cluster in the F2 populations. Consequently, these new-type lines represent a significant new source of genetic diversity. As a practical application, we introgressed clubroot resistance from the European fodder turnip ECD04 ( ) into using the hexaploid bridge strategy coupled with MAS. Over four selection cycles (F2 to F5), the donor allele frequency surged from 31.3% to 54.4%, showing a strong negative correlation with disease severity (r = -0.98) and yielding highly resistant F5 lines. This study demonstrates that the hexaploid bridge strategy enables rapid genetic base broadening and efficient trait improvement in .

Clubroot, caused by Plasmodiophora brassicae , is a significant disease affecting brassica crops worldwide and poses a threat to canola ( Brassica napus ) production in western Canada. Management of this disease heavily relies on the use of resistant cultivars, but resistance erosion is a serious concern due to the highly diverse pathogen populations. Understanding resistance mechanisms may aid in better deployment/rotation of clubroot resistance (CR) genes and improve resistance resilience. In this study, we conducted a comparative analysis using resistant canola varieties carrying either a single ( Rcr1 ) or double CR genes ( Rcr1 + Crr1 rutb ) to decipher the resistance modes associated with these genes. Cell wall (CW) biopolymeric compounds in different root layers were mapped and quantified using Fourier-transform mid-infrared microspectroscopy for changes in CW elements associated with clubroot resistance. Transmission electron and confocal microscopy were used to assess root infection details and relative transcript abundance was analyzed to determine the activation of the lignin-related pathway in relation to resistance. Neither resistant variety affected the primary infection of root hairs/epidermal cells compared to the susceptible “Westar”, but both exhibited strong inhibition of cortical infection, effectively ‘trapping’ the pathogen in the exodermis. The most prominent change observed was increased lignin accumulation associated with resistance. In Westar, the pathogen was able to degrade CW lignin, facilitating access to the root cortex by secondary plasmodia of P . brassicae . In contrast, resistant varieties showed clear lignin accumulation around the penetration site on the exodermis, accompanied by elevated expression of genes involved in the phenylpropanoid pathway. These results suggest that induced lignin accumulation plays a role in clubroot resistance mediated by the CR genes Rcr1 and Crr1 rutb in canola, providing cellular and structural evidence that supports the data from earlier transcriptomic studies.

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.