Abstract
Plasmodiophora brassicae is a protozoan pathogen that causes clubroot disease in cruciferous plants, particularly Chinese cabbage (Brassica rapa). A previous study identified a clubroot resistance gene (CRd) conferring race-specific resistance to P. brassicae. However, the defense mechanisms of B. rapa against virulent vs. avirulent P. brassicae are poorly understood. In this study, we carried out a global transcriptional analysis in the clubroot-resistant Chinese cabbage inbred line “85–74” carrying the CRd gene and inoculated with avirulent (LAB-4) or virulent (SCCD-52) P. brassicae. RNA sequencing showed that “85–74” responded most rapidly to SCCD-52 infection, and the number of differentially expressed genes was much higher in SCCD-52-treated as compared to LAB-4-treated plants (5552 vs. 304). Transcriptome profiling revealed that plant hormone signal transduction and plant–pathogen interaction pathways played key roles in the late stages of P. brassicae infection. Genes relating to the salicyclic acid (SA), jasmonic acid (JA)/ethylene (ET), and brassinosteroid (BR) signaling pathways were up-regulated relative to untreated plants in response to LAB-4 infection at 8, 16, and 32 days post-inoculation (dpi) whereas JA, ET, and BR signaling-related genes were not activated in response to SCCD-52, and SA signaling-related genes were up-regulated in both LAB-4 and SCCD-52, suggesting that SA signaling is not the key factor in host resistance to avirulent P. brassicae. In addition, genes associated with phosphorylation and Ca2+ signaling pathways were down-regulated to a greater degree following LAB-4 as compared to SCCD-52 infection at 8 dpi. These results indicate that effector-triggered immunity in “85–74” is more potently activated in response to infection with avirulent P. brassicae and that JA, ET, and BR signaling are important for the host response at the late stage of infection. These findings provide insight into P. brassicae pathotype-specific defense mechanisms in cruciferous crops.
Highlights
Plants have evolved immune responses consisting of initial pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and subsequent effector-triggered immunity (ETI) [1] for protection against pathogens such as bacteria, viruses, and fungi [1,2,3,4]
Genes relating to the salicyclic acid (SA), jasmonic acid (JA)/ethylene (ET), and brassinosteroid (BR) signaling pathways were up-regulated relative to untreated plants in response to LAB-4 infection at 8, 16, and 32 days post-inoculation whereas JA, ET, and BR signaling-related genes were not activated in response to SCCD-52, and SA signaling-related genes were up-regulated in both LAB-4 and SCCD-52, suggesting that SA signaling is not the key factor in host resistance to avirulent P. brassicae
These results indicate that effector-triggered immunity in “85–74” is more potently activated in response to infection with avirulent P. brassicae and that JA, ET, and BR signaling are important for the host response at the late stage of infection
Summary
Plants have evolved immune responses consisting of initial pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and subsequent effector-triggered immunity (ETI) [1] for protection against pathogens such as bacteria, viruses, and fungi [1,2,3,4]. Agronomy 2019, 9, 589 intracellular receptors encoded by plant disease resistance genes (R genes) that recognize the effector protein and subsequently activate downstream immune responses to prevent pathogen infection [5]. The SA pathway is required for plant resistance to specific necrotrophic pathogens (Plectosphaerella cucumerina), while ET and JA signaling mediate resistance to some biotrophic pathogens (Pseudomonas syringae and Peronospora parasitica) [13,14]
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