Natural variation in a FtMYB32 ‐ FtCES18 module drives Rhizoctonia solani resistance by reprogramming jasmonate and flavonoid metabolism in Tartary buckwheat
10 affiliations
- 1Sanya Nan Fan Research Institute of Chinese Academy of Agricultural Sciences Sanya Hainan 572024 China
- 2Hainan Seed Industry Laboratory Sanya 572024 China
- 3State Key Laboratory of Crop Gene Resources and Breeding, Institute of Crop Sciences Chinese Academy of Agricultural Sciences Beijing 100081 China
- 4College of Agriculture Yangtze University Jingzhou Hubei 434023 China
- 5School of Life and Health Sciences Hunan University of Science and Technology Xiangtan Hunan 411201 China
- 6Alliance of Bioversity International and CIAT New Delhi India
- 7School of Life Sciences Royal Global University Guwahati India
- 8Skolkovo Institute of Science and Technology Moscow Russia
- 9Vavilov Institute of General Genetics Russian Academy of Science Moscow Russia
- 10Institute of Economic Crops Henan Academy of Agricultural Sciences Zhengzhou 450003 China
Abstract
SUMMARY: Tartary buckwheat (Fagopyrum tataricum) is renowned for its adaptability to complex growing conditions and stress tolerance. However, soil‐borne necrotrophic pathogens such as Rhizoctonia solani frequently cause devastating diseases that severely compromise its yield and quality. In this study, through a genome‐wide association study (GWAS), we identified a carboxylesterase gene, FtCES18, and demonstrated that it acts as a core positive regulator of disease resistance in Tartary buckwheat. Overexpression of FtCES18 significantly enhanced plant resistance, whereas virus‐induced gene silencing (VIGS) led to a highly susceptible phenotype. Further analyses revealed that FtCES18 efficiently catalyzes the hydrolysis of methyl jasmonate (MeJA) into free jasmonic acid (JA), which initiates downstream JA‐Ile signaling and rapidly promotes endogenous jasmonate accumulation upon pathogen infection. This JA signaling cascade reprograms host flavonoid metabolism, promoting the substantial accumulation of downstream defensive flavonoids (such as rutin and quercetin). Furthermore, we found that the transcription factor FtMYB32 directly binds to the MBS cis‐element in the FtCES18 promoter to activate its expression. Notably, evolutionary analysis revealed a domestication‐associated C‐terminal truncation in the cultivated FtMYB32 that impairs its transactivation capacity, explaining the compromised basal resistance in cultivated accessions compared to their wild ancestors. Crucially, a natural single‐nucleotide polymorphism (SNP) in the FtMYB32 promoter defines a superior haplotype (hapC) conferring enhanced basal transcriptional activity. This natural variation in promoter activity controls the expression abundance of the FtMYB32‐FtCES18 module via a “dosage fine‐tuning” effect, which is subsequently amplified by the downstream metabolic cascade, ultimately contributing to the natural variation in disease resistance among different Tartary buckwheat accessions. This study provides valuable genetic resources and a theoretical basis for breeding novel Tartary buckwheat varieties with high disease resistance.
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BibTeX
@article{chen2026natural,
title = {{Natural variation in a FtMYB32 ‐ FtCES18 module drives Rhizoctonia solani resistance by reprogramming jasmonate and flavonoid metabolism in Tartary buckwheat}},
author = {Yuanyuan Chen and Yang Liu and Xixu Peng and Haihua Wang and Zhengwu Fang and Jai Chand Rana and Nikhil Chrungoo and Maria D Logachev and Chaonan Guan and Meiliang Zhou},
journal = {The Plant Journal},
year = {2026},
month = oct,
doi = {10.1111/tpj.71176},
url = {https://doi.org/10.1111/tpj.71176},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Natural variation in a FtMYB32 ‐ FtCES18 module drives Rhizoctonia solani resistance by reprogramming jasmonate and flavonoid metabolism in Tartary buckwheat
AU - Yuanyuan Chen
AU - Yang Liu
AU - Xixu Peng
AU - Haihua Wang
AU - Zhengwu Fang
AU - Jai Chand Rana
AU - Nikhil Chrungoo
AU - Maria D Logachev
AU - Chaonan Guan
AU - Meiliang Zhou
PY - 2026
DA - 2026/10/01
JO - The Plant Journal
DO - 10.1111/tpj.71176
UR - https://doi.org/10.1111/tpj.71176
AB - SUMMARY: Tartary buckwheat (Fagopyrum tataricum) is renowned for its adaptability to complex growing conditions and stress tolerance. However, soil‐borne necrotrophic pathogens such as Rhizoctonia solani frequently cause devastating diseases that severely compromise its yield and quality. In this study, through a genome‐wide association study (GWAS), we identified a carboxylesterase gene, FtCES18, and demonstrated that it acts as a core positive regulator of disease resistance in Tartary buckwheat. Overexpression of FtCES18 significantly enhanced plant resistance, whereas virus‐induced gene silencing (VIGS) led to a highly susceptible phenotype. Further analyses revealed that FtCES18 efficiently catalyzes the hydrolysis of methyl jasmonate (MeJA) into free jasmonic acid (JA), which initiates downstream JA‐Ile signaling and rapidly promotes endogenous jasmonate accumulation upon pathogen infection. This JA signaling cascade reprograms host flavonoid metabolism, promoting the substantial accumulation of downstream defensive flavonoids (such as rutin and quercetin). Furthermore, we found that the transcription factor FtMYB32 directly binds to the MBS cis‐element in the FtCES18 promoter to activate its expression. Notably, evolutionary analysis revealed a domestication‐associated C‐terminal truncation in the cultivated FtMYB32 that impairs its transactivation capacity, explaining the compromised basal resistance in cultivated accessions compared to their wild ancestors. Crucially, a natural single‐nucleotide polymorphism (SNP) in the FtMYB32 promoter defines a superior haplotype (hapC) conferring enhanced basal transcriptional activity. This natural variation in promoter activity controls the expression abundance of the FtMYB32‐FtCES18 module via a “dosage fine‐tuning” effect, which is subsequently amplified by the downstream metabolic cascade, ultimately contributing to the natural variation in disease resistance among different Tartary buckwheat accessions. This study provides valuable genetic resources and a theoretical basis for breeding novel Tartary buckwheat varieties with high disease resistance.
SN - 0960-7412
SN - 1365-313X
ER -