Geminivirus satellite-encoded beta C1 activates UPR, induces bZIP60 nuclear export, and manipulates the expression of bZIP60 downstream genes to benefit virus infection

文献类型： 外文期刊

第一作者： Zhang, Mingzhen

作者： Zhang, Mingzhen;Cao, Buwei;Zhou, Xueping;Li, Fangfang;Zhang, Mingzhen;Fan, Zaifeng;Zhang, Hui;Zhou, Xueping

作者机构：

关键词： geminivirus; beta C1; unfolded protein response (UPR); bZIP60; nuclear export

期刊名称：SCIENCE CHINA-LIFE SCIENCES （ 影响因子：10.372； 五年影响因子：7.587 ）

ISSN： 1674-7305

年卷期：

页码：

收录情况： SCI

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 TYLCCNB beta C1 is a major inducer of UPR and can upregulate the expression of bZIP60, a transcription factor in Nicotiana benthamiana plants. Treatment using ER stress inducers or overexpression of NbbZIP60 increases beta C1 accumulation and benefits TYLCCNV/TYLCCNB infection in N. benthamiana plants, and vice versa. In the TYLCCNV/TYLCCNB-infected or the beta C1-expressin g cells, NbbZIP60 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 NbbZIP60-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 NbbZIP60 to evade plant defense response, which is a distinct virulence strategy exploited by plant pathogens.

分类号：

  • 相关文献
作者其他论文 更多>>

微信小程序