BjuA03.BNT1 plays a positive role in resistance to clubroot disease in resynthesized Brassica juncea L.

文献类型： 外文期刊

第一作者： Li, Keqi

作者： Li, Keqi;Wang, Kai;Shi, Yiji;Liang, Fenghao;Li, Xinru;Bao, Shunjun;Yesmagul, Balziya Maratkyzy;Fatima, Maliha;Yu, Chengyu;Xu, Aixia;Zhang, Xingguo;Shi, Xue;Huang, Zhen;Zhou, Zhaoyong;Dun, Xiaoling;Fu, Sanxiong

作者机构：

关键词： Brassica juncea; Clubroot; Plasmodiophora brassica; QTL; BjuA03.BNT1

期刊名称：PLANT SCIENCE （ 影响因子：4.1； 五年影响因子：5.1 ）

ISSN： 0168-9452

年卷期： 2024 年 349 卷

页码：

收录情况： SCI

摘要： Clubroot has become a major obstacle in rapeseed production. Breeding varieties resistant to clubroot is the most effective method for disease management. However, the clubroot-resistant germplasm of rapeseed remains limited. To tackle this challenge, we synthesized the clubroot-resistant mustard, CT19, via distant hybridization, and subsequently an F-2 segregating population was created by intercrossing CT19 with a clubroot-susceptible germplasm CS15. A major-effect clubroot resistance QTL qCRa3-1 on chromosome A03 was identified through QTL scanning. Transcriptome analyses of CT19 and CS15 revealed that the mechanisms conferring resistance to Plasmodiophora brassica likely involved the regulation of flavonoid metabolism, fatty acid metabolism, and sulfur metabolism. By combining the results from transcriptome, QTL mapping, and gene sequencing, a candidate gene BjuA03.BNT1, encoding NLR (nucleotide-binding domain leucine-rich repeat-containing receptors) protein, was obtained. Intriguingly, comparing with CT19, a base T insertion was discovered in the BjuA03.BNT1 gene's coding sequence in CS15, resulting an alteration within the LRR conserved domain. Overexpression of BjuA03.BNT1 from CT19 notably enhanced the resistance to clubroot in Arabidopsis. Our investigations revealed that BjuA03.BNT1 regulated the resistance to clubroot by modulating fatty acid synthesis and the structure of cell wall. These results are highly relevant for molecular breeding to improve clubroot resistance in rapeseed.

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