Viral proteins resolve the virus-vector conundrum during hemipteran-mediated transmission by subverting salicylic acid signaling pathway

Jing-Ru Zhang, Yi-Ming Liu, Di Li, Yi-Jie Wu, Shi-Xing Zhao, Xiao-Wei Wang, Shu-Sheng Liu, Linda L. Walling and Li-Long Pan ()
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Jing-Ru Zhang: Zhejiang University
Yi-Ming Liu: Zhejiang University
Di Li: Zhejiang University
Yi-Jie Wu: Zhejiang University
Shi-Xing Zhao: Zhejiang University
Xiao-Wei Wang: Zhejiang University
Shu-Sheng Liu: Zhejiang University
Linda L. Walling: University of California
Li-Long Pan: Zhejiang University

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract 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.

Date: 2024
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DOI: 10.1038/s41467-024-53894-y

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