Editing strigolactone hormone receptor for robust antiviral silencing in rice
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, Y. Ji, Yi Li, Jie Zhang, Liming Yan, Shou‐Wei Ding, Shanshan Zhao, Jianguo Wu
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.