福建农林大学吴建国课题组近日取得一项新成果。经过不懈努力，他们的研究开发出了在水稻中编辑独角曲内酯激素受体，实现抗病毒的强效沉默。相关论文于2026年2月24日发表在《细胞》杂志上。
研究人员发现，独角麦内酯（SL）激素信号通过RNA依赖性RNA聚合酶1（RDR1）和RDR6的转录激活促进水稻植株抗病毒沉默。该研究团队证明了水稻草矮病毒（RGSV）的蛋白P3通过直接隔离受体DWARF14和DWARF3来阻断SL信号传导。P3-DWARF14复合物的结构和功能分析表明，DWARF14 102位（D102）的天冬氨酸对P3相互作用至关重要，但对SL感知并不重要。
值得注意的是，通过胞嘧啶碱基编辑（CBE）将DWARF14的一个D102N替换引入两个水稻品种中，通过阻断病毒对SL信号依赖性抗病毒沉默的抑制，赋予了对RGSV的抗性。他们的发现建立了一种无转基因的抗病工程策略，通过对SL受体进行精确的基因组编辑，以逃避病原体对内源性防御途径的抑制。
据了解，小干扰RNA （siRNA）途径通过RNA沉默指导广谱抗病毒防御，因此毒性感染需要有效抑制防御机制。
附：英文原文
Title: Editing strigolactone hormone receptor for robust antiviral silencing in rice
Author: Guoyi Yang, Ming Wu, Shuai Zhang, Yucen Huang, Yixiao Liu, Xiyuan Yu, Jiayang Hu, Le Mi, Peng Gan, Yuansheng Wu, Jing Zou, Baogang Zhang, Qun Hu, Jie Hu, Ruifeng Yao, Bojian Zhong, Xianbo Huang, Huiting Xie, Yinghua Ji, Yi Li, Jie Zhang, Liming Yan, Shou-wei Ding, Shanshan Zhao, Jianguo Wu
Issue&Volume: 2026-02-24
Abstract: The small interfering RNA (siRNA) pathway directs broad-spectrum antiviral defense through RNA silencing so that virulent infection requires efficient suppression of the defense mechanism. Here, we show that strigolactone (SL) hormone signaling promotes antiviral silencing in rice plants by transcriptional activation of RNA-dependent RNA polymerase 1 (RDR1) and RDR6. We demonstrate that protein P3 of the rice grassy stunt virus (RGSV) blocks SL signaling by directly sequestering the receptor DWARF14 from DWARF3. Structural and functional analyses of the P3-DWARF14 complex reveal that the aspartic acid at position 102 (D102) of DWARF14 is essential for the P3 interaction but not for SL perception. Notably, a single D102N substitution of DWARF14, introduced into two rice cultivars by cytosine base editing (CBE) confers resistance against RGSV by blocking viral suppression of SL signaling-dependent antiviral silencing. Our findings establish a transgene-free strategy for engineering disease resistance by precise genome editing of the SL receptor to escape pathogen suppression of the endogenous defense pathway.
DOI: 10.1016/j.cell.2026.01.013
Source: https://www.cell.com/cell/abstract/S0092-8674(26)00100-5