TCP19 regulates nitrogen-dependent sheath blight susceptibility by modulating nitrogen uptake and signalling in rice

文献类型： 外文期刊

第一作者： Zhou, Tiange

作者： Zhou, Tiange;Chen, Huan;Zhu, Hongyao;Xuan, Yuan Hu;Zhou, Tiange;Chen, Huan;Zhu, Hongyao;Xuan, Yuan Hu;Zhou, Tiange;Zhu, Hongyao;Zhu, Xiaofeng;Chen, Huan;Jiang, Xu;Jung, Ki-Hong;Jiang, Xu;Jung, Ki-Hong;Lin, Qiujun

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关键词： nitrogen; TCP19; PIL15; IDD10; N signalling; rice

期刊名称：PLANT BIOTECHNOLOGY JOURNAL （ 影响因子：10.5； 五年影响因子：12.4 ）

ISSN： 1467-7644

年卷期： 2025 年 23 卷 9 期

页码：

收录情况： SCI

摘要： The excessive application of nitrogen fertilization improves rice yield, but increases disease severity. However, the underlying molecular mechanisms remain unclear. Here, we conducted a comparative analysis of nitrogen- and R. solani-regulated transcriptomes and identified TEOSINTE BRANCHED, CYC, PCF 19 (TCP19), that was a key regulator of nitrogen use efficiency (NUE), as a potential link between nitrogen metabolism and sheath blight (ShB) regulation. Inoculation of tcp19 and TCP19 OXs with R. solani revealed that TCP19 negatively regulated ShB resistance independent of nitrogen conditions. TCP19 expression was suppressed under moderate nitrogen (MN) but induced under high nitrogen (HN) conditions. Furthermore, TCP19 directly activated Dense and Erect Panicle 1 (DEP1) while repressing nitrate transporter 1.1B (NRT1.1B), ammonium transporter 1;2 (AMT1;2) and pathogenesis-related 1b (PR1b). Notably, TCP19 induced by HN conditions further strengthened this regulation. Phytochrome interacting factor like protein 15 (PIL15), a TCP19 interactor, directly activated DEP1 and AMT1;2 while repressing NRT1.1B. Additionally, the key nitrogen signalling regulator Indeterminate domain 10 (IDD10) interacted with both TCP19 and PIL15 and inhibited DEP1 activation by TCP19 and PIL15. Interestingly, DEP1 competitively interacted with IDD10 to release TCP19 and PIL15. Overall, our findings elucidate the mechanisms by which TCP19 regulates nitrogen signalling in rice ShB resistance, highlighting TCP19-PR1b signal under HN conditions as a key factor contributing to increased disease severity.

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