Plasmodiophora brassicae CBM18 Proteins Bind Chitin and Suppress Chitin-Triggered Immunity

Abstract

Plants have a sophisticated and multilayered immune system. However, plant pathogens, helped by effector proteins, have found several strategies to evade plant immunity. For instance, the clubroot pathogen Plasmodiophora brassicae is able to turn the roots of susceptible hosts into nutrient-sink galls suppressing pattern-triggered immunity (PTI) and effector-triggered immunity. Chitin, the main component of P. brassicae spore cell walls and a well-known pathogen-associated molecular pattern, can elicit PTI but is also the target of plant chitinases and chitin deacetylases. The fact that P. brassicae does not trigger PTI during infection of susceptible hosts motivated a genome-wide search of genes coding for secreted proteins with domains previously associated with chitin binding. We found that the P. brassicae genome encodes a repertoire of candidate-secreted effectors containing the chitin-binding domain carbohydrate-binding module family 18 (CBM18), chitinase, and chitin deacetylase domains. The role of these proteins in the pathogenicity of the clubroot pathogen is unknown. Here, we characterized two CBM18 proteins, PbChiB2 and PbChiB4, which are transcriptionally activated during infection. Through coprecipitation, we found that recombinant PbChiB2 and PbChiB4 bind to spores and to chitin oligomers. We also showed that both proteins suppress chitin-triggered activation of the map kinase proteins MPK3 and MPK6 in the host Brassica napus. These findings suggest that P. brassicae CBM18 proteins act as effectors for protecting the clubroot pathogen and for suppressing chitin-triggered immunity during infection. [Graphic: see text] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Keywords

• chitin-binding protein
• clubroot
• canola
• effectors
• chitin-triggered immunity