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Aphanomyces root rot (ARR), caused by Aphanomyces euteiches Drechs., is a destructive soilborne disease of eld pea (Pisum Sativum L.). No completely resistant pea germplasm is available, and current ARR management strategies rely on partial resistance and fungicidal seed treatments. In this study, an F 8 recombinant inbred line (RIL) population of 135 individuals from the cross 'Reward' (susceptible) × '00-2067' (tolerant) was evaluated for reaction to ARR under greenhouse conditions with the A. euteiches isolate Ae-MDCR1 and over 2 years in a eld nursery in Morden, Manitoba. Root rot severity, foliar weight, plant vigor and height were used as estimates of tolerance to ARR. Genotyping was conducted with a 13.2K single-nucleotide polymorphism (SNP) array and 222 simple sequence repeat (SSR) markers. Statistical analyses of the phenotypic data indicated signi cant (P<0.001) genotypic effects and signi cant G×E interactions (P<0.05) in all experiments. After ltering, 3050 (23.1%) of the SNP and 30 (13.5%) of the SSR markers were retained for linkage analysis, which distributed 2999 (2978 SNP + 21 SSR) of the markers onto nine linkage groups representing the seven chromosomes of pea. Mapping of quantitative trait loci (QTL) identi ed 5 major-effect (R 2 > 20%), 13 moderate-effect (10%

Clubroot disease caused by the soil-borne pathogen Plasmodiophora brassicae Woronin is a major threat to the production of Brassica crops worldwide. The European winter canola cv. 'Mendel' shows resistance to many P. brassicae isolates including pathotypes 3, 5, 6 and 8 that are prevalent in Canada. To introgress clubroot resistance (CR) into Canadian spring Brassica napus canola, crosses between Canadian spring and European winter B. napus canola cv. 'Mendel' were made and several resistant lines were developed through pedigree breeding. Two of the resistant lines were further crossed with the clubroot susceptible spring canola line A07-26NR to produce two doubled haploid (DH) populations from nine F 1 plants. Segregation for resistance followed a 1:1 ratio for resistant and susceptible phenotypes suggesting that a single Mendelian gene is involved in the control of resistance to P. brassicae single spore isolate SACAN-ss1 (pathotype 3) in the DH population where the 'favourable allele' for resistance is derived from the cv. 'Mendel'. Genetic and physical mapping study positioned five previously described CR loci (CRk, Crr3, CRb, CRa and CRb Kato ) on the B. rapa chromosome A3, and identified twelve markers (1.5-2.0 % recombination) from the genomic region that houses the CRa and CRb Kato loci to be associated with the resistance derived from 'Mendel'. The identified markers can be used in breeding as well as pyramiding of multiple clubroot resistance genes.

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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.