Geminivirus satellite-encoded βC1 activates UPR,induces bZIP60 nuclear export,and manipulates the expression of bZIP60 downstream genes to benefit virus infection  

作　　者：Mingzhen Zhang Buwei Cao Hui Zhang Zaifeng Fan Xueping Zhou Fangfang Li 

机构地区：[1]State Key Laboratory for Biology of Plant Diseases and Insect Pests,Institute of Plant Protection,Chinese Academy of Agricultural Sciences,Beijing,100193,China [2]State Key Laboratory of Agro-Biotechnology and Key Laboratory of Pest Monitoring and Green Management-MARA,China Agricultural University,Beijing,100193,China [3]Horticultural Research Institute,Shanghai Academy of Agricultural Sciences,Shanghai,201403,China [4]State Key Laboratory of Rice Biology,Institute of Biotechnology,Zhejiang University,Hangzhou,310058,China

出　　处：《Science China(Life Sciences)》2023年第6期1408-1425,共18页中国科学（生命科学英文版）

基　　金：supported by the National Key Research and Development Program of China (2021YFD1400400);the National Natural Science Foundation of China (32172385,31930089)。

摘　　要：UPR is a conserved response in eukaryotes and can alleviate endoplasmic reticulum(ER)stresses induced by abiotic and biotic stresses.The interactions between UPR and plant RNA viruses have been documented,while the interplays between UPR and plant DNA viruses remain unknown.Using tomato yellow leaf curl China virus(TYLCCNV)and its associated betasatellite(TYLCCNB)as a model,we indicate that TYLCCNBβC1 is a major inducer of UPR and can upregulate the expression of b ZIP60,a transcription factor in Nicotiana benthamiana plants.Treatment using ER stress inducers or overexpression of Nbb ZIP60 increasesβC1 accumulation and benefits TYLCCNV/TYLCCNB infection in N.benthamiana plants,and vice versa.In the TYLCCNV/TYLCCNB-infected or theβC1-expressing cells,Nbb ZIP60 is exported from the nucleus to the nuclear periphery via the XPO1 pathway,and blocking the XPO1 pathway inhibited TYLCCNV/TYLCCNB infection.We have found that the Nbb ZIP60-regulated pro-survival genes could promote virus infection,and the pro-death gene plays a contrasting role in virus infection.This study reveals that geminivirus infection activates UPR and utilizes the up-regulated molecular chaperons to promote viral infection,and then induces the nuclear export of Nbb ZIP60 to evade plant defense response,which is a distinct virulence strategy exploited by plant pathogens.

关 键 词：GEMINIVIRUS βC1 unfolded protein response(UPR) bZIP60 nuclear export 

分 类 号：S432.41[农业科学—植物病理学]