Scholay

学术搜索 · AI 审稿 · LaTeX 协作

TaWRKY24 integrates the tryptophan metabolism pathways to participate in defense against Fusarium crown rot in wheat

作者:Xing Xu, Tai‐Fei Yu, Ji‐Tong Wei, Xiaofei Ma, Yongwei Liu, Jinpeng Zhang, Lei Zheng, Zehao Hou, Jun Chen, Yongbin Zhou, Ming Chen, Jian Ma, Yunfeng Jiang, Hanhua Ji, Lihui Li, You‐Zhi Ma, Zhi‐An Zhang, Zhao‐Shi Xu · 发表于:The Plant Journal · 年份:2024 · DOI:10.1111/tpj.17079 · 被引用次数:24 · 研究领域:Plant Gene Expression Analysis、Plant-Microbe Interactions and Immunity、Plant Pathogens and Fungal Diseases

Wheat growth process has been experiencing severe challenges arising from the adverse environment. Notably, the incidence of Fusarium crown rot (FCR), a severe soil-borne disease caused by Fusarium pseudograminearum (Fp), has significantly intensified in various wheat-growing regions, resulting in a decline in grain yield. However, the identification of wheat varieties and the exploration of effective gene resources resistant to FCR have not yet been accomplished. Here, we screened and identified the tryptophan metabolism pathway to participate in wheat resistance to FCR by correlation analysis between transcriptome and metabolome, and found that indole-3-acetaldehyde (IAAld) and melatonin, two key metabolites in the tryptophan metabolic pathway, were significantly accumulated in Fp-induced wheat stem bases. Interestingly, exogenous application of these two metabolites could significantly enhance wheat resistance against Fp. Additionally, we observed that the activity of TaALDHase, a crucial enzyme responsible for catalyzing IAAld to produce indole-3-acetic acid (IAA), was inhibited. Conversely, the activity of TaMTase, a rate-limiting involved in melatonin biosynthesis, was enhanced in the Fp-induced wheat transcriptome. Further analysis showed that TaWRKY24 could regulate IAA and melatonin biosynthesis by inhibiting the expression of TaALDHase and enhancing the transcription of TaMTase, respectively. Silencing of TaALDHase could significantly increase wheat resistance to FC...