斯里兰卡木薯花叶病毒AC2与拟南芥SGS3蛋白互作研究OA北大核心CSTPCD

Cassava mosaic disease(CMD)poses a serious threat and danger to cassava production in China and the world,and there is no effective control method and lack of resistant materials,causing serious economic losses,and is considered one of the most threatening viral diseases.Sri Lankan cassava mosaic virus(SLCMV)is one of the major pathogens causing cassava mosaic disease.RNA silencing is an innate antiviral immune response mechanism in plants and animals,and post transcriptional gene silencing(PTGS)is a conserved gene expression regulatory mechanism in eukaryotes,and is one of the important antiviral immune mechanisms.Suppressor of gene silencing 3(SGS3)is a key protein of the PTGS pathway and plays a critical role in host defense against viral invasion.To counteract this host immune response,viruses usually encode viral suppressors of RNA silencing(VSRs)to counteract the viral defense mechanism of host PTGS,and interaction with host proteins is one of the main mechanisms of action for the silencing suppressors to function.In order to investigate whether SLCMV AC2 inhibits the immune function of host PTGS by interacting with AtSGS3,we analyzed the immune function of host PTGS by using yeast two-hybrid(Y2H)system and bimolecular fluorescence complementation(BiFC)experiments,to analyze the interaction between AtSGS3 and SLCMV AC2.The results showed that SLCMV AC2 interacted with AtSGS3 protein in both yeast cells and plants.In subcellular co-localization experimental studies,we further demonstrated that SLCMV AC2 could co-localize with AtRDR6,a close partner of AtSGS3,after interacting with AtSGS3.The data suggest that SLCMV AC2 may affect the host autoimmune mechanism and enhance viral pathogenicity by interacting with siRNA-body,and that the interaction between SLCMV AC2 and AtSGS3 may be the molecular basis for the development of foliar symptoms in SLCMV-infected cassava,and the results of this study would provide a new theoretical basis for the subsequent in-depth analysis of the pathogenicity mechanism of SLCMV.