Geminiviruses are widespread across the globe and cause devastating diseases in food and medicinal crops.Their C3 proteins have long been known to enhance viral replication;however,the underlying molecular mechanisms ...Geminiviruses are widespread across the globe and cause devastating diseases in food and medicinal crops.Their C3 proteins have long been known to enhance viral replication;however,the underlying molecular mechanisms remain poorly understood.In this study,we show that transgenic plants overexpressing the C3 protein of tobacco curly shoot geminivirus(TbCSV)exhibit hypersensitive responses to cytokinin(CK)treatment,which largely restores the attenuated viral replication observed in the TbCSV C3 mutant(TbCSV_(mC3)).We identified NbTAF12b,a negative regulator of CK signaling in Nicotiana benthamiana,as a C3-interacting protein that attenuates TbCSV replication.TbCSV C3 not only inhibits the transcription of NbTAF12b but also competes with NbRR1 and NbKMD17 for binding to the NbTAF12b protein.This competition disrupts the formation of the NbTAF12b-NbKMD-NbRR heterotrimer and promotes NbRR1 accumulation,thereby enhancing CK signaling and ultimately facilitating TbCSV replication.C3 proteins from other distantly related geminiviruses exhibit similar 3D structures and also target NbTAF12b in vivo,suggesting that this mechanism is conserved among geminiviruses.These findings shed new light on the molecular mechanism by which TbCSV C3 facilitates viral replication through the modulation of CK signaling and provide potential molecular targets for engineering virus-resistant plants.展开更多
The nonstructural protein 1 （NS1） of influenza A virus, which is absent from the viral particle, but highly expressed in infected cells, strongly antagonizes the interferon （IFN）-mediated antiviral response. We en...The nonstructural protein 1 （NS1） of influenza A virus, which is absent from the viral particle, but highly expressed in infected cells, strongly antagonizes the interferon （IFN）-mediated antiviral response. We engineered an NS1-expressing 293 （293-NS1） cell line with no response to IFN stimulation. Compared with the parental 293 cells,展开更多
基金financially supported by the Natural Science Foundation of China(32272482 and U20A2037)the National Key R&D Plan in China(2024YFD1400702)+2 种基金the Talent Project of Zhejiang Province(2019R52033)the Key Research and Development Program of Zhejiang Province(2019C02018)the Innovation Research 2035 Pilot Plan of Southwest University(SWU-XDZD22002).
文摘Geminiviruses are widespread across the globe and cause devastating diseases in food and medicinal crops.Their C3 proteins have long been known to enhance viral replication;however,the underlying molecular mechanisms remain poorly understood.In this study,we show that transgenic plants overexpressing the C3 protein of tobacco curly shoot geminivirus(TbCSV)exhibit hypersensitive responses to cytokinin(CK)treatment,which largely restores the attenuated viral replication observed in the TbCSV C3 mutant(TbCSV_(mC3)).We identified NbTAF12b,a negative regulator of CK signaling in Nicotiana benthamiana,as a C3-interacting protein that attenuates TbCSV replication.TbCSV C3 not only inhibits the transcription of NbTAF12b but also competes with NbRR1 and NbKMD17 for binding to the NbTAF12b protein.This competition disrupts the formation of the NbTAF12b-NbKMD-NbRR heterotrimer and promotes NbRR1 accumulation,thereby enhancing CK signaling and ultimately facilitating TbCSV replication.C3 proteins from other distantly related geminiviruses exhibit similar 3D structures and also target NbTAF12b in vivo,suggesting that this mechanism is conserved among geminiviruses.These findings shed new light on the molecular mechanism by which TbCSV C3 facilitates viral replication through the modulation of CK signaling and provide potential molecular targets for engineering virus-resistant plants.
基金supported by China Mega-Project for Infectious Disease(2014ZX10004002-004-001)National Natural Science Foundation of China(31500152)National Key Technology R&D Program(2014BAI13B04)
文摘The nonstructural protein 1 （NS1） of influenza A virus, which is absent from the viral particle, but highly expressed in infected cells, strongly antagonizes the interferon （IFN）-mediated antiviral response. We engineered an NS1-expressing 293 （293-NS1） cell line with no response to IFN stimulation. Compared with the parental 293 cells,
