Abstract
Gall formation on the belowground parts of plants infected with Plasmodiophora brassicae is the result of extensive host cellular reprogramming. The development of these structures is a consequence of increased cell proliferation followed by massive enlargement of cells colonized with the pathogen. Drastic changes in cellular growth patterns create local deformities in the roots and hypocotyl giving rise to mechanical tensions within the tissue of these organs. Host cell wall extensibility and recomposition accompany the growth of the gall and influence pathogen spread and also pathogen life cycle progression. Demethylation of pectin within the extracellular matrix may play an important role in P. brassicae-driven hypertrophy of host underground organs. Through proteomic analysis of the cell wall, we identified proteins accumulating in the galls developing on the underground parts of Arabidopsis thaliana plants infected with P. brassicae. One of the key proteins identified was the pectin methylesterase (PME18); we further characterized its expression and conducted functional and anatomic studies in the knockout mutant and used Raman spectroscopy to study the status of pectin in P. brassicae-infected galls. We found that late stages of gall formation are accompanied with increased levels of PME18. We have also shown that the massive enlargement of cells colonized with P. brassicae coincides with decreases in pectin methylation. In pme18-2 knockout mutants, P. brassicae could still induce demethylation; however, the galls in this line were smaller and cellular expansion was less pronounced. Alteration in pectin demethylation in the host resulted in changes in pathogen distribution and slowed down disease progression. To conclude, P. brassicae-driven host organ hypertrophy observed during clubroot disease is accompanied by pectin demethylation in the extracellular matrix. The pathogen hijacks endogenous host mechanisms involved in cell wall loosening to create an optimal cellular environment for completion of its life cycle and eventual release of resting spores facilitated by degradation of demethylated pectin polymers.
Highlights
Clubroot disease, caused by the protist pathogen Plasmodiophora brassicae, is responsible for extensive damage to oilseed rape and brassica vegetable crops
Accumulation of extracellular proteins during the expansive growth of galls in P. brassicae-infected Arabidopsis hypocotyls was investigated by two-dimensional gel electrophoresis (2D GE)
Protein samples isolated from cell walls of non-infected and infected (20 days after infection (DAI) and 26 DAI) samples were subjected to isoelectric focusing on pH gradient 6–10 and resolution by SDS-PAGE
Summary
Clubroot disease, caused by the protist pathogen Plasmodiophora brassicae, is responsible for extensive damage to oilseed rape and brassica vegetable crops. Cellular reprograming in the underground parts of plants allows the pathogen to acquire host nutrients and secure space for resting spore formation (Malinowski et al, 2019). Enormous growth of pathogen-colonized cells and local cell wall decomposition that accompanies the emergence of secondary plasmodia, followed by resting spore formation and maturation, is a characteristic symptom of the clubroot disease (Gustafsson et al, 1986). Schuller et al (2014) proposed that this response may be mediated by auxin-brassinosteroid crosstalk, disturbance of which leads to changes in pathogen distribution and development. Host organ hypertrophy provides space for the pathogen and elevates cellular metabolism, redirecting nutrient distribution and source sink relations within the plant (Chandran et al, 2010; Bragança et al, 2016; Walerowski et al, 2018). The capacity of pathogens to enzymatically degrade cell walls of the host influences their infectivity and release back to the environment (Walton, 1994)
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