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SLR1-LPA1信号调控水稻对纹枯病的抗性及叶片夹角。

SLR1-LPA1 signal regulates sheath blight resistance and lamina joint angle in rice.

作者信息

Zhu Hongyao, Chen Huan, Kantharaj Vimalraj, Sun Wenpeng, Wei Songhong, Xuan Yuan Hu

机构信息

College of Plant Protection, Shenyang Agricultural University, Shenyang, 110866, China.

Institute of Agriculture and Life Science (IALS), Gyeongsang National University, Jinju, 52828, Republic of Korea.

出版信息

Plant Physiol Biochem. 2025 May;222:109689. doi: 10.1016/j.plaphy.2025.109689. Epub 2025 Feb 25.

Abstract

Previous studies have suggested that Dense and Erect Panicle 1 (DEP1) interacts with Lose Plant Architecture 1 (LPA1) to regulate auxin transport by which DEP1-LPA1 modulates rice sheath blight (ShB) resistance. In this study, we identified that dep1 and lpa1 exhibited semi-dwarfism and dep1/lpa1 was shorter than the single mutant. LPA1 OX displayed higher height, whereas DEP1 OX exhibited similar height with wild-type. The gibberellic acid (GA)-dependent shoot growth was inhibited in dep1 and lpa1 while activated in LPA1 OX, suggesting that LPA1 may play a role in GA signaling transduction. Yeast two-hybrid screening revealed that slender rice 1 (SLR1), a GA signaling negative regulator, interacted with LPA1. Additionally, slr1 was less susceptible to ShB, whereas the GA signaling positive regulator DWARF1 mutant d1 was more susceptible to ShB. This suggested that GA signaling positively regulates rice resistance to ShB. Furthermore, slr1 was similar to LPA1 OX in terms of reduced lamina joint angle, whereas d1 did not show any difference. This implied that SLR1 may regulate LPA1 dependent signaling to control the lamina joint angle via a mechanism that was independent of GA signaling. Transcriptome data indicated that GA signaling and catabolic genes were regulated by LPA1. Transient and ChIP assays suggested that LPA1 bound to the promoter of gibberellin 2-beta-dioxygenase, a GA catabolic gene, to activate its expression. These findings indicated that LPA1 modulated GA homeostasis and SLR1 interacted with and inhibited LPA1 to regulate ShB resistance and lamina joint angle in rice.

摘要

先前的研究表明,密穗直立穗1(DEP1)与松散株型1(LPA1)相互作用以调节生长素运输,DEP1-LPA1通过该过程调节水稻纹枯病(ShB)抗性。在本研究中,我们发现dep1和lpa1表现出半矮化,且dep1/lpa1比单突变体更矮。LPA1过表达(LPA1 OX)表现出更高的株高,而DEP1过表达(DEP1 OX)与野生型株高相似。dep1和lpa1中赤霉素(GA)依赖性的地上部生长受到抑制,而在LPA1 OX中被激活,这表明LPA1可能在GA信号转导中发挥作用。酵母双杂交筛选显示,GA信号负调控因子细长水稻1(SLR1)与LPA1相互作用。此外,slr1对ShB的敏感性较低,而GA信号正调控因子矮化1(DWARF1)突变体d1对ShB更敏感。这表明GA信号正向调节水稻对ShB的抗性。此外,slr1在叶片夹角减小方面与LPA1 OX相似,而d1没有表现出任何差异。这意味着SLR1可能通过一种独立于GA信号的机制调节LPA1依赖性信号来控制叶片夹角。转录组数据表明,GA信号和分解代谢基因受LPA1调控。瞬时和染色质免疫沉淀(ChIP)分析表明,LPA1与GA分解代谢基因赤霉素2-β-双加氧酶的启动子结合以激活其表达。这些发现表明,LPA1调节GA稳态,SLR1与LPA1相互作用并抑制LPA1以调节水稻对ShB的抗性和叶片夹角。

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