Unveiling effector-triggered immunity by Plasmodiophora brassicae as a source of durable clubroot disease resistance

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Canola industry and the production of cruciferous vegetables in Canada and worldwide has a common enemy: Plasmodiophora brassicae, the clubroot pathogen of the crucifers. P. brassicae is an intracellular protist responsible for millions in losses worldwide. In the last 10 years, clubroot has cost to the canola industry only, around $500 million in losses. The use of resistant varieties has been a key strategy to avoid the damages caused by the pathogen. Over the years, the resistance has been rapidly overcome by new pathotypes of P. brassicae highlighting the need to identify durable sources of resistance. During the infection process, many plant pathogens such as P. brassicae release effector proteins that can suppress plant immunity and allow disease progression. In return, plants have evolved defense mechanisms known as effector-triggered immunity (ETI). This layer of immunity plays a key role in protecting specific plant genotypes against specific pathogen races through intracellular receptors that possess nucleotide-binding leucine-rich repeat (NLR) domains, which recognize pathogen effectors. Effectors conserved among pathogen strains, termed core effectors, have been used as probes to screen for new NLRs to incorporate into breeding programs to generate resistant plants. Recently, different subsets of P. brassicae effectors have been reported, but to date P. brassicae core effectors have yet to be identified. We plan to define P. brassicae core effectors among the different pathotypes identified worldwide using their genomic sequences. We further plan to determine their functionality to elicit ETI (i.e., ETI-eliciting effectors) using the Arabidopsis thaliana-P. brassicae pathosystem model. To unveil this mechanism for P. brassicae, we seek to fulfill the following objectives: 1) to characterize P. brassicae core effectors in terms of degree of conservation among pathotypes and structure of protein families; 2) to identify P. brassicae effectors interacting with A. thaliana NLRs; 3) to identify A. thaliana NLRs associated with P. brassicae effectors; and 4) to determine if those A. thaliana NLRs mediating the interaction with P. brassicae effectors are also present in other Brassica crops. Achieving these objectives will provide original contributions to the understanding of P. brassicae biology and the mechanisms used by the clubroot pathogen to establish infection in the susceptible host. In the longer term, this will lead to the development of plants resistant to P. brassicae and to an environmentally friendly and less costly management of the clubroot disease.