文献类型： 外文期刊

第一作者： Zhao, Wenhao

作者： Zhao, Wenhao;Zhou, Yijun;Ji, Yinghua;Zhao, Wenhao;Wang, Xiaofeng;Zhou, Xueping;Zhou, Xueping

作者机构：

期刊名称：PLOS PATHOGENS （ 影响因子：6.823； 五年影响因子：7.455 ）

ISSN： 1553-7366

年卷期： 2021 年 17 卷 8 期

页码：

收录情况： SCI

摘要： Author summary Geminiviruses infect numerous crops, induce a wide range of symptoms, and cause tremendous crop losses annually. Tomato yellow leaf curl virus (TYLCV), a single-component geminivirus, is a causative agent leading to one of the most devastating tomato diseases in the world. As a single-stranded DNA virus, genomic replication occurs in the nucleus and therefore, the nuclear shuttling is a critical step of viral infection. The V2 protein of TYLCV is involved in symptom development and viral trafficking, among other steps, and hijacks host proteins for executing its functions. Nevertheless, host factors involved in the V2-mediated functions are not well addressed. We show that tomato GRXC6 (SlGRXC6) functions as a restriction factor of TYLCV infection by interacting with and preventing V2 from moving out of the nucleus, leading to the inhibited V2-mediated nuclear export of V1 and the V1-viral DNA complex. SlGRXC6 also contributes to symptom development via its interaction with NTRC80. V2 sequesters SlGRXC6 from forming the SlGRXC6-SlNTRC80 complex and regulates plant growth. Our work, therefore, identified a new host partner of V2 and revealed the mechanisms whereby V2 functions as a pathogenicity determinant and can be targeted for virus control. Geminiviruses cause serious symptoms and devastating losses in crop plants. With a circular, single-stranded DNA genome, geminiviruses multiply their genomic DNA in the nucleus, requiring the nuclear shuttling of viral proteins and viral genomic DNAs. Many host factors, acting as proviral or antiviral factors, play key roles in geminivirus infections. Here, we report the roles of a tomato glutaredoxin (GRX), SlGRXC6, in the infection of Tomato yellow leaf curl virus (TYLCV), a single-component geminivirus. The V2 protein of TYLCV specifically and preferentially interacts with SlGRXC6 among the 55-member tomato GRX family that are broadly involved in oxidative stress responses, plant development, and pathogen responses. We show that overexpressed SlGRXC6 increases the nuclear accumulation of V2 by inhibiting its nuclear export and, in turn, inhibits trafficking of the V1 protein and viral genomic DNA. Conversely, the silenced expression of SlGRXC6 leads to an enhanced susceptibility to TYLCV. SlGRXC6 is also involved in symptom development as we observed a positive correlation where overexpression of SlGRXC6 promotes while knockdown of SlGRXC6 expression inhibits plant growth. We further showed that SlGRXC6 works with SlNTRC80, a tomato NADPH-dependent thioredoxin reductase, to regulate plant growth. V2 didn't interact with SlNTRC80 but competed with SlNTR80 for binding to SlGRXC6, suggesting that the V2-disrupted SlGRXC6-SlNTRC80 interaction is partially responsible for the virus-caused symptoms. These results suggest that SlGRXC6 functions as a host restriction factor that inhibits the nuclear trafficking of viral components and point out a new way to control TYLCV infection by targeting the V2-SlGRXC6 interaction.

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