Tomato leaf curl Yunnan virus-encoded C4 induces cell division through enhancing stability of Cyclin D 1.1 via impairing NbSK eta-mediated phosphorylation in Nicotiana benthamiana

文献类型： 外文期刊

第一作者： Huang, Changjun

作者： Huang, Changjun;Zhou, Xueping;Yang, Xiuling;Zhou, Xueping;Huang, Changjun;Zhang, Xiuren;Huang, Changjun;Zhang, Xiuren

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： 2018 年 14 卷 1 期

页码：

收录情况： SCI

摘要： The whitefly-transmitted geminiviruses induce severe developmental abnormalities in plants. Geminivirus-encoded C4 protein functions as one of viral symptom determinants that could induce abnormal cell division. However, the molecular mechanism by which C4 contributes to cell division induction remains unclear. Here we report that tomato leaf curl Yunnan virus (TLCYnV) C4 interacts with a glycogen synthase kinase 3 (GSK3)/SHAGGY-like kinase, designed NbSK eta, in Nicotiana benthamiana. Pro32, Asn34 and Thr35 of TLCYnV C4 are critical for its interaction with NbSK eta and required for C4-induced typical symptoms. Interestingly, TLCYnV C4 directs NbSK eta to the membrane and reduces the nuclear-accumulation of NbSK eta. The relocalization of NbSK eta impairs phosphorylation dependent degradation on its substrate-Cyclin D1.1 (NbCycD1;1), thereby increasing the accumulation level of NbCycD1; 1 and inducing the cell division. Moreover, NbSK eta-RNAi, 35S::NbCycD1;1 transgenic N. benthamiana plants have the similar phenotype as 35S::C4 transgenic N. benthamiana plants on callus-like tissue formation resulted from abnormal cell division induction. Thus, this study provides new insights into mechanism of how a viral protein hijacks NbSK eta to induce abnormal cell division in plants.

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