Tomato yellow leaf curl virus intergenic siRNAs target a host long noncoding RNA to modulate disease symptoms

文献类型： 外文期刊

第一作者： Yang, Yuwen

作者： Yang, Yuwen;Liu, Tingli;Wang, Jinyan;Ling, Xitie;Hu, Zhongze;Chen, Tianzi;Hu, Jieli;Huang, Junyu;Yu, Wengui;Zhang, Baolong;Shen, Danyu;Dou, Daolong;Wang, Ming-Bo

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： 2019 年 15 卷 1 期

页码：

收录情况： SCI

摘要： Tomato yellow leaf curl virus (TYLCV) and its related begomoviruses cause fast-spreading diseases in tomato worldwide. How this virus induces diseases remains largely unclear. Here we report a noncoding RNA-mediated model to elucidate the molecular mechanisms of TYLCV-tomato interaction and disease development. The circular ssDNA genome of TYLCV contains a noncoding intergenic region (IR), which is known to mediate viral DNA replication and transcription in host cells, but has not been reported to contribute directly to viral disease development. We demonstrate that the IR is transcribed in dual orientations during plant infection and confers abnormal phenotypes in tomato independently of protein-coding regions of the viral genome. We show that the IR sequence has a 25-nt segment that is almost perfectly complementary to a long noncoding RNA (lncRNA, designated as SlLNR1) in TYLCV-susceptible tomato cultivars but not in resistant cultivars which contains a 14-nt deletion in the 25-nt region. Consequently, we show that viral small-interfering RNAs (vsRNAs) derived from the 25-nt IR sequence induces silencing of SlLNR1 in susceptible tomato plants but not resistant plants, and this SlLNR1 downregulation is associated with stunted and curled leaf phenotypes reminiscent of TYLCV symptoms. These results suggest that the lncRNA interacts with the IR-derived vsRNAs to control disease development during TYLCV infection. Consistent with its possible function in virus disease development, over-expression of SlLNR1 in tomato reduces the accumulation of TYLCV. Furthermore, gene silencing of the SlLNR1 in the tomato plants induced TYLCV-like leaf phenotypes without viral infection. Our results uncover a previously unknown interaction between vsRNAs and host lncRNA, and provide a plausible model for TYLCV-induced diseases and host antiviral immunity, which would help to develop effective strategies for the control of this important viral pathogen. Author summary Tomato yellow leaf curl virus (TYLCV) is an important threat to tomato production worldwide. Six resistance/tolerance genes (Ty) have been introgressed from wild tomato species for breeding against the virus and some of them confer tolerance to TYLCV by enhancing gene silencing. Here, we propose a novel model for TYLCV-induced symptoms and host antiviral immunity, which is independent of the known Ty genes. We show that the virus-derived vsRNAs may cause abnormal phenotypes similar to virus infection by targeting and regulating a lncRNA (designated as SlLNR1) in tomato. Furthermore, we find that SlLNR1 contributes to the normal development and TYLCV resistance in tomato. Interestingly, SlLNR1 exhibits a natural variant in a tomato cultivar that may evade vsRNAs-mediated cleavage. Thus, we suggest a novel evolutionary arms race between the vsRNAs and lncRNA, which could open new avenues in developing new viral control strategies.

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