CLCuMuB beta C1 Subverts Ubiquitination by Interacting with NbSKP1s to Enhance Geminivirus Infection in Nicotiana benthamiana

文献类型： 外文期刊

第一作者： Jia, Qi

作者： Jia, Qi;Liu, Na;Xie, Ke;Dai, Yanwan;Han, Shaojie;Zhao, Xijuan;Qian, Lichao;Wang, Yunjing;Zhao, Jinping;Xie, Daoxin;Liu, Yule;Dai, Yanwan;Zhao, Jinping;Gorovits, Rena;Hong, Yiguo

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： 2016 年 12 卷 6 期

页码：

收录情况： SCI

摘要： Viruses interfere with and usurp host machinery and circumvent defense responses to create a suitable cellular environment for successful infection. This is usually achieved through interactions between viral proteins and host factors. Geminiviruses are a group of plant-infecting DNA viruses, of which some contain a betasatellite, known as DNA beta. Here, we report that Cotton leaf curl Multan virus (CLCuMuV) uses its sole satellite-encoded protein beta C1 to regulate the plant ubiquitination pathway for effective infection. We found that CLCuMu betasatellite (CLCuMuB) beta C1 interacts with NbSKP1, and interrupts the interaction of NbSKP1s with NbCUL1. Silencing of either NbSKP1s or NbCUL1 enhances the accumulation of CLCuMuV genomic DNA and results in severe disease symptoms in plants. beta C1 impairs the integrity of SCFCOI1 and the stabilization of GAI, a substrate of the SCFSYL1 to hinder responses to jasmonates (JA) and gibberellins (GA). Moreover, JA treatment reduces viral accumulation and symptoms. These results suggest that CLCuMuB beta C1 inhibits the ubiquitination function of SCF E3 ligases through interacting with NbSKP1s to enhance CLCuMuV infection and symptom induction in plants.

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