Chinese Bulletin of Botany ›› 2026, Vol. 61 ›› Issue (3): 357-368.DOI: 10.3724/CBB-2026-0044

• SPOTLIGHT • Previous Articles    

Precision Engineering of Strigolactone Receptor Aids Rice in Antiviral Defense

Jinhua Yang, Bing Wang*   

  1. State Key Laboratory of Seed Innovation, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China

  • Online:2026-05-10 Published:2026-05-20
  • Contact: Bing Wang

Abstract: The RNA interference (RNAi) pathway acts as a conserved and broad-spectrum antiviral defense mechanism in plants, whereas viruses deploy effector proteins to counter host defense. Strigolactones (SLs) are a new class of phytohormones that regulate plant architecture, stress resilience, arbuscular mycorrhizal symbiosis, and parasitic diseases, but their antiviral mechanisms remain unclear. Recent research reveals that SL signaling is a pivotal regulatory node in the arms race between viruses and plants. SLs induce the expression of the transcription factor ONAC131, which acts synergistically with the virus-responsive protein MID1 to enhance antiviral RNAi. However, the rice grassy stunt virus (RGSV) deploys the P3 effector to dampen SL perception by disrupting the interaction between the SL receptor D14 and D3, thereby weakening the antiviral defense of rice. Precise editing of D14 remarkably enhances resistance to RGSV without yield penalty. This work reveals a novel mechanism whereby the SL signaling pathway and the RNAi pathway cooperate to counter viral invasion. It also provides a precise target for antiviral breeding in crops and represents a major breakthrough in the field of plant virology. In light of this, this paper summarizes the research progress on the antiviral RNAi pathway and SL signaling pathway, highlighting the regulatory functions of SL and other phytohormone signaling pathways in the offensive and defensive interactions between plants and viruses. Looking ahead, it offers new insights for the targeted breeding of antiviral crops by identifying key genes in hormone signaling hubs.