Ministry of Agriculture Key Lab of Molecular Biology of Crop Pathogens and Insects, Zhejiang Key Laboratory of Biology and Ecological Regulation of Crop Pathogens and Insects, Institute of Insect Sciences, Zhejiang University, 310058, Hangzhou, China.
Department of Botany and Plant Sciences, Center for Plant Cell Biology, University of California, 92521-0124, Riverside, USA.
Nat Commun. 2024 Nov 1;15(1):9448. doi: 10.1038/s41467-024-53894-y.
Hemipteran insects transmit viruses when infesting plants, during which vectors activate salicylic acid (SA)-regulated antiviral defenses. How vector-borne plant viruses circumvent these antiviral defenses is largely unexplored. During co-infections of begomoviruses and betasatellites in plants, betasatellite-encoded βC1 proteins interfere with SA signaling and reduce the activation of antiviral resistance. βC1 inhibits SA-induced degradation of NbNPR3 (Nicotiana benthamiana nonexpressor of pathogenesis-related genes 3), a negative regulator of SA signaling. βC1 does not bind directly to NbNPR3, but regulates NbNPR3 degradation via heat shock protein 90s (NbHSP90s). NbHSP90s bind to both NbNPR3 and βC1 and suppress SA signaling. This viral success strategy appears to be conserved as it is also documented for viral proteins encoded by two aphid-borne viruses. Our findings reveal an exquisite mechanism that facilitates the persistence of vector-borne plant viruses and provide important insights into the intricacies of the virus life cycle.
半翅目昆虫在侵害植物时会传播病毒，在此期间，载体会激活水杨酸（SA）调节的抗病毒防御。载体传播的植物病毒如何规避这些抗病毒防御在很大程度上尚不清楚。在植物中双生病毒和β卫星病毒的共同感染中，β卫星编码的βC1 蛋白干扰 SA 信号转导并降低抗病毒抗性的激活。βC1 抑制 SA 诱导的 NbNPR3（Nicotiana benthamiana nonexpressor of pathogenesis-related genes 3）的降解，NbNPR3 是 SA 信号转导的负调节剂。βC1 不直接与 NbNPR3 结合，而是通过热休克蛋白 90s（NbHSP90s）调节 NbNPR3 的降解。NbHSP90s 结合 NbNPR3 和 βC1 并抑制 SA 信号转导。这种病毒成功策略似乎是保守的，因为它也记录在两种蚜虫传播的病毒编码的病毒蛋白中。我们的研究结果揭示了一种精致的机制，有助于载体传播的植物病毒的持续存在，并为病毒生命周期的复杂性提供了重要的见解。
