Strigolactone signaling: Licensing antiviral RNA interference in rice

Abstract

Strigolactone (SL) signaling is well recognized for its regulation of plant architecture; however, its involvement in antiviral immunity has remained unclear. In a recent study, Yang et al. uncovered an unexpected role of SL signaling in promoting antiviral RNA interference (RNAi) in rice. They showed that SL signaling enhances the transcription of RNA‐dependent RNA polymerases RDR1 and RDR6 via the ONAC131‐MID1 transcriptional module, thereby amplifying the production of virus‐derived small interfering RNAs (vsiRNAs) and conferring broad‐spectrum antiviral resistance. In counter‐defense, the rice grassy stunt virus (RGSV) deploys its effector protein P3 to bind the SL receptor DWARF14 (D14), competitively blocking the recruitment of the F‐box protein D3 and suppressing SL‐mediated antiviral silencing. Guided by the cryo‐EM structure of the P3‐D14 complex, the authors introduced a single amino acid substitution (D102N) in D14 using cytosine base editing. This precise modification abolishes P3 binding while maintaining normal SL perception and downstream signaling. The edited rice lines exhibit strong field resistance to RGSV without compromising yield or agronomic traits. This work establishes a transgene‐free strategy for engineering stable antiviral resistance by precisely editing a hormone receptor to evade pathogen suppression, providing a conceptual framework for precision crop breeding.