文献类型： 外文期刊

第一作者： Sun, Shaoshuang

作者： Sun, Shaoshuang;Li, Shupeng;Zhou, Xueping;Yang, Xiuling;Zhou, Xueping

作者机构：

期刊名称：PLOS PATHOGENS （ 影响因子：6.7； 五年影响因子：6.7 ）

ISSN： 1553-7366

年卷期： 2023 年 19 卷 4 期

页码：

收录情况： SCI

摘要： Author summaryPlants employ multiple layers of antiviral defense to fight against geminivirus infection. Transcription factors are key masters that can reprogram transcription and enable plant to respond to different stimuli adequately and flexibly. Here we explore the molecular basis of the NbWRKY1 transcription factor in regulating geminivirus infection. We provide evidence that NbWRKY1 positively regulates plant defense response against geminivirus. We also identify that NbWRKY1 binds to the promoter of the NbWHIRLY1 (NbWhy1) transcription factor and represses the transcription of NbWhy1. Furthermore, we show that NbWhy1 is a negative regulator of antiviral RNAi defense and interferes with the interaction of calmodulin 3 and calmodulin-binding transcription activator-3 to promote geminivirus infection. Collectively, this study reveals that NbWRKY1 represses NbWhy1 to positively regulate plant defense to geminivirus infection. WHIRLY transcription factors have been previously described to a positive regulatory role in basal and induced defense responses in Arabidopsis, but their roles in plant virus infection remains exclusive. Our study demonstrates a pro-viral role of NbWhy1 in geminivirus infection, expanding our knowledge of the NbWRKY1-NbWhy1 cascade during plant-geminivirus interaction. Geminiviruses constitute the largest group of known plant viruses and cause devastating diseases and economic losses in many crops worldwide. Due to limited naturally occurring resistance genes, understanding plant antiviral defense against geminiviruses is critical for finding host factors of geminiviruses and development of strategies for geminivirus control. Here we identified NbWRKY1 as a positive regulator of plant defense against geminivirus infection. Using tomato yellow leaf curl China virus/tomato yellow leaf curl China betasatellite (TYLCCNV/TYLCCNB) as a representative geminivirus, we found that NbWRKY1 was upregulated in response to TYLCCNV/TYLCCNB infection. Overexpression of NbWRKY1 attenuated TYLCCNV/TYLCCNB infection, whereas knockdown of NbWRKY1 enhanced plant susceptibility to TYLCCNV/TYLCCNB. We further revealed that NbWRKY1 bound to the promoter of the NbWHIRLY1 (NbWhy1) transcription factor and inhibited the transcription of NbWhy1. Consistently, NbWhy1 negatively regulates plant response against TYLCCNV/TYLCCNB. Overexpression of NbWhy1 significantly accelerated TYLCCNV/TYLCCNB infection. Conversely, knockdown of NbWhy1 led to impaired geminivirus infection. Furthermore, we demonstrated that NbWhy1 interfered with the antiviral RNAi defense and disrupted the interaction between calmodulin 3 and calmodulin-binding transcription activator-3. Moreover, the NbWRKY1-NbWhy1 also confers plant antiviral response toward tomato yellow leaf curl virus infection. Taken together, our findings suggest that NbWRKY1 positively regulates plant defense to geminivirus infection by repressing NbWhy1. We propose that the NbWRKY1-NbWhy1 cascade could be further employed to control geminiviruses.

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