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Review
. 2025 Feb;26(2):e70060.
doi: 10.1111/mpp.70060.

Constructing a Novel Disease Resistance Mechanism Model for Cruciferous Crops: An Example From Black Rot

Affiliations
Review

Constructing a Novel Disease Resistance Mechanism Model for Cruciferous Crops: An Example From Black Rot

Haojie Dai et al. Mol Plant Pathol. 2025 Feb.

Abstract

Cruciferous crops are essential components of global agricultural production due to their rich nutritional value and extensive economic benefits. Black rot caused by Xanthomonas campestris pv. campestris (Xcc) has caused significant losses to cruciferous crops. Therefore, studying the resistance mechanisms of cruciferous crops to improve the disease resistance of cruciferous crops is of significant practical importance. This review introduces the biological characteristics and epidemiological patterns of the Xcc. The main resistance mechanisms including the physical barrier functions, immune responses, systemic resistance, regulation of photosynthesis, antimicrobial effects of secondary metabolites, production and regulation of reactive oxygen species, and the signalling pathways of salicylic acid, jasmonic acid and ethylene of cruciferous crops to Xcc are also summarised. Comprehensive knowledge of these resistance mechanisms will provide theoretical support for enhancing disease resistance in crops.

Keywords: Xanthomonas campestris pv. campestris; black rot; cruciferous crops; resistant mechanisms.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Pathogenic mechanism of Xanthomonas campestris pv. campestris (Xcc) colonisation in the vascular system. Upon invading the plant, Xcc colonises the vascular bundles and employs the type III secretion system (T3SS) to release effector proteins (T3Es) that suppress the plant's immune response. It subsequently secretes extracellular polysaccharides (EPS), which obstruct the vascular bundles and diminish the vitality of surrounding cells. Simultaneously, Xcc secretes extracellular enzymes using the type II secretion system (T2SS) that degrade the plant cell wall, facilitating the release of nutrients to fuel its own growth. Image created with BioRender.com, with permission.
FIGURE 2
FIGURE 2
The signal transduction process of Xanthomonas campestris pv. campestris (Xcc) in plants. After completing colonisation, Xcc initiates systemic expansion and reproduction, using quorum sensing (QS) and a two‐component signal transduction system (TCS) to regulate population density throughout this process. DSF, diffusion signal factor; P, phosphate; RR, response regulator; SK, sensor kinase. Image created with BioRender.com, with permission.
FIGURE 3
FIGURE 3
Barrier effect of cell wall and wax layer. During Xanthomonas campestris pv. campestris (Xcc) invasion, the cell wall and wax layer serve as crucial physical barriers. The cell wall, rich in lignin and cellulose, effectively resists Xcc's entry. Additionally, wall‐associated kinases (WAKs) located on the cell wall play a key role in signalling; when the cell wall is damaged, WAKs transmit signals that activate the upregulation of resistance genes. ISR, induced systemic resistance; JA, jasmonic acid; SA, salicylic acid; SAR, systemic acquired resistance. Image created with BioRender.com, with permission.
FIGURE 4
FIGURE 4
Main resistance mechanisms of cruciferous crops to Xanthomonas campestris pv. campestris (Xcc). The primary resistance mechanism is the immune response, which is divided into pathogen‐associated molecular pattern (PAMP)‐triggered immunity (PTI) and effector‐triggered immunity (ETI). PTI is initiated by bacterial molecular patterns and exhibits broad‐spectrum defence, involving reactive oxygen species (ROS), secondary metabolites, hormones, and modulation of photosynthesis. ETI is triggered by specific bacterial effectors and often leads to a strong hypersensitive response (HR). AP, antimicrobial peptide; CAPE, cysteine‐rich antimicrobial peptide; CDPK, calcium‐dependent protein kinase; ET, ethylene; HLP, Hevein‐like protein; ISR, induced systemic resistance; GHP, glucosyl hydrolysis product; GSL, glucosinolate; JA, jasmonic acid; PA, phenolic acid; POD, peroxidase; PRR, pattern recognition receptor; PR, pathogenesis‐related protein; PSI, photosystem I; PSII, photosystem II; SA, salicylic acid; SAR, systemic acquired resistance; T3E, type III effector; T3SS, type III secretion system; TF, transcription factor. Image created with BioRender.com, with permission.

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