Loss of PMR4 callose synthase triggers jasmonic acid–dependent resistance to the clubroot disease in Arabidopsis and Brassica napus
4 affiliations
- 1Department of Biochemistry, Microbiology and Immunology, University of Saskatchewan , Saskatoon, SK , S7N 5E5
- 2Department of Plant Sciences, University of Saskatchewan , Saskatoon, SK , S7N 5A8
- 3Agriculture and Agri-Food Canada, Saskatoon Research and Development Centre , Saskatoon, SK , S7N 0X2
- 4Department of Biology, University of Saskatchewan , Saskatoon, SK , S7N 5E2
Abstract
Clubroot caused by the protist pathogen Plasmodiophora brassicae Woronin is a major disease in Brassicaceae crops. Growing clubroot-resistant cultivars remains the most effective and practical control strategy, but diverse or emerging pathotypes can often overcome resistance genes deployed. In this study, we identified POWDERY MILDEW RESISTANT 4 (PMR4) as a potential host susceptibility factor that can be targeted as a novel genetic resource for durable clubroot resistance. Recessive PMR4 mutations in Arabidopsis thaliana conferred strong resistance to multiple P. brassicae pathotypes, independent of salicylic acid-mediated plant immunity. Using CRISPR/Cas9, we edited 2 PMR4 orthologs in the Brassica napus genome, and the resulting homozygous mutants exhibited resistance to both powdery mildew and clubroot diseases. This study reveals that P. brassicae infection induces callose deposition in Arabidopsis and B. napus roots in a PMR4-dependent manner, similar to wound- and powdery mildew-induced callose deposition in Arabidopsis leaves. The Arabidopsis pmr4-1 mutation does not affect P. brassicae primary infection but blocks the pathogen entry from epidermal cells to the stele in a jasmonic acid signaling-dependent manner, which coincides with accumulation of lignin-like and suberin compounds in periderm cell walls. Together, these findings establish PMR4-encoded callose synthase as a host susceptibility factor facilitating secondary infection by P. brassicae and demonstrate its potential as a gene-editing target for enhancing resistance to powdery mildew, clubroot, and possibly other biotic and abiotic stresses in Brassicaceae crops.
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BibTeX
@article{luo2026loss,
title = {{Loss of PMR4 callose synthase triggers jasmonic acid–dependent resistance to the clubroot disease in Arabidopsis and Brassica napus}},
author = {Runbang Luo and Lipu Wang and Rui Wen and Kun Yang and Xunjia Liu and Peng Gao and J. C. Tu and Tim Dumonceaux and Yangdou Wei and Gary Peng and Wei Xiao},
journal = {The Plant Cell},
year = {2026},
month = jun,
doi = {10.1093/plcell/koag160},
url = {https://doi.org/10.1093/plcell/koag160},
note = {CC BY},
}
RIS
TY - JOUR
TI - Loss of PMR4 callose synthase triggers jasmonic acid–dependent resistance to the clubroot disease in Arabidopsis and Brassica napus
AU - Runbang Luo
AU - Lipu Wang
AU - Rui Wen
AU - Kun Yang
AU - Xunjia Liu
AU - Peng Gao
AU - J. C. Tu
AU - Tim Dumonceaux
AU - Yangdou Wei
AU - Gary Peng
AU - Wei Xiao
PY - 2026
DA - 2026/06/01
JO - The Plant Cell
DO - 10.1093/plcell/koag160
UR - https://doi.org/10.1093/plcell/koag160
AB - Clubroot caused by the protist pathogen Plasmodiophora brassicae Woronin is a major disease in Brassicaceae crops. Growing clubroot-resistant cultivars remains the most effective and practical control strategy, but diverse or emerging pathotypes can often overcome resistance genes deployed. In this study, we identified POWDERY MILDEW RESISTANT 4 (PMR4) as a potential host susceptibility factor that can be targeted as a novel genetic resource for durable clubroot resistance. Recessive PMR4 mutations in Arabidopsis thaliana conferred strong resistance to multiple P. brassicae pathotypes, independent of salicylic acid-mediated plant immunity. Using CRISPR/Cas9, we edited 2 PMR4 orthologs in the Brassica napus genome, and the resulting homozygous mutants exhibited resistance to both powdery mildew and clubroot diseases. This study reveals that P. brassicae infection induces callose deposition in Arabidopsis and B. napus roots in a PMR4-dependent manner, similar to wound- and powdery mildew-induced callose deposition in Arabidopsis leaves. The Arabidopsis pmr4-1 mutation does not affect P. brassicae primary infection but blocks the pathogen entry from epidermal cells to the stele in a jasmonic acid signaling-dependent manner, which coincides with accumulation of lignin-like and suberin compounds in periderm cell walls. Together, these findings establish PMR4-encoded callose synthase as a host susceptibility factor facilitating secondary infection by P. brassicae and demonstrate its potential as a gene-editing target for enhancing resistance to powdery mildew, clubroot, and possibly other biotic and abiotic stresses in Brassicaceae crops.
SN - 1040-4651
SN - 1532-298X
ER -