Abstract
Clubroot, caused by Plasmodiophora brassicae, is one of the most important diseases of canola (Brassica napus) in Canada. Disease management relies heavily on planting clubroot resistant (CR) cultivars, but in recent years, new resistance-breaking pathotypes of P. brassicae have emerged. Current efforts against the disease are concentrated in developing host resistance using traditional genetic breeding, omics and molecular biology. However, because of its obligate biotrophic nature, limited resources have been dedicated to investigating molecular mechanisms of pathogenic infection. We previously performed a transcriptomic study with the cultivar resistance-breaking pathotype 5X on two B. napus hosts presenting contrasting resistance/susceptibility, where we evaluated the mechanisms of host response. Since cultivar-pathotype interactions are very specific, and pathotype 5X is one of the most relevant resistance-breaking pathotypes in Canada, in this study, we analyze the expression of genes encoding putative secreted proteins from this pathotype, predicted using a bioinformatics pipeline, protein modeling and orthologous comparisons with effectors from other pathosystems. While host responses were found to differ markedly in our previous study, many common effectors are found in the pathogen while infecting both hosts, and the gene response among biological pathogen replicates seems more consistent in the effectors associated with the susceptible interaction, especially at 21 days after inoculation. The predicted effectors indicate the predominance of proteins with interacting domains (e.g., ankyrin), and genes bearing kinase and NUDIX domains, but also proteins with protective action against reactive oxygen species from the host. Many of these genes confirm previous predictions from other clubroot studies. A benzoic acid/SA methyltransferase (BSMT), which methylates SA to render it inactive, showed high levels of expression in the interactions with both hosts. Interestingly, our data indicate that E3 ubiquitin proteasome elements are also potentially involved in pathogenesis. Finally, a gene with similarity to indole-3-acetaldehyde dehydrogenase is a promising candidate effector because of its involvement in indole acetic acid synthesis, since auxin is one of the major players in clubroot development.
Highlights
Clubroot disease, which results from infection by the soilborne obligate parasite Plasmodiophora brassicae Wor., causes significant damage to plants in the Brassicaceae family, and to crops of agricultural importance like canola (Brassica napus L.) (Dixon, 2009)
There were no differentially expressed genes at 7 dai when comparing P. brassicae transcripts coming from infection of the resistant host genotype ‘Laurentian’ vs. the susceptible genotype ‘Brutor.’ This could be due to a lower number of pathogenic cells at the beginning of secondary infection, which was demonstrated by lack of symptoms in the both host genotypes at this time point (Galindo-González et al, 2020)
The transcript corresponding to this protein showed the highest relative abundance (TPM) from the differentially expressed secreted genes (DESGs) at 21 dai in P. brassicae cells from the two host genotypes, but with an opposite trend with the gene being more abundant in P. brassicae infecting ‘Laurentian.’ The transcript levels of SPQ95221.1, as calculated by TPM, decreased in P. brassicae infecting ‘Laurentian’ from 29758.99 at 14 dai to 26366.57 at 21 dai
Summary
Clubroot disease, which results from infection by the soilborne obligate parasite Plasmodiophora brassicae Wor., causes significant damage to plants in the Brassicaceae family, and to crops of agricultural importance like canola (Brassica napus L.) (Dixon, 2009). The emergence of new pathotypes of P. brassicae (Strelkov et al, 2016, 2018; Hollman et al, 2021) is related to crop management practices and selection pressure on the pathogen, reflecting the arms race between the molecular defense mechanisms of the host and the generation of pathogen effectors utilized to overcome resistance. The resting spores germinate to produce primary zoospores, which invade host root hairs and epidermal cells to generate primary plasmodia. These cleave into zoosporangia, from which secondary zoospores are released back into the soil. Increased root growth aids in housing the enlarged secondary plasmodia and provides a sink for nutrients utilized by the pathogen, and it is likely that most of the molecular interactions between host and pathogen take place during this stage, making this phase relevant in effector secretion and pathogenesis (Pérez-López et al, 2020, 2021)
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