C4, the Pathogenic Determinant of Tomato Leaf Curl Guangdong Virus, May Suppress Post-transcriptional Gene Silencing by Interacting With BAM1 Protein
C4, the Pathogenic Determinant of Tomato Leaf Curl Guangdong Virus, May Suppress Post-transcriptional Gene Silencing by Interacting With BAM1 Protein
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C4是广东番茄卷叶病毒的致病决定因素，可能通过与BAM1蛋白相互作用来抑制转录后基因沉默
DOI：
10.3389/fmicb.2020.00851
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发表时间：
2020-05-05
影响因子：
5.2
通讯作者：
He, Zifu
中科院分区：
文献类型：
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作者：
Li, Zhenggang;Du, Zhenguo;He, Zifu
广东番茄曲叶病毒（Tomato Leaf Curl Guangdong Virus，ToLCGdV）是一种与广东省番茄黄化曲叶病（Tomato yellow leaf curl disease，TYLCD）有关的菜豆病毒。作为双生病毒蛋白中最不保守的蛋白，C4在ToLCGdV感染过程中的功能尚未阐明。本研究构建了ToLCGdV的感染性克隆和C4 ORF缺失的ToLCGdV突变体（ToLCGdVmC 4）。虽然ToLCGdV和ToLCGdVmC 4可以侵染烟草和番茄植株，但ToLCGdVmC 4引起的症状比ToLCGdV轻得多。为了进一步验证C4在病毒致病中的作用，我们在N.本塞姆氏马铃薯病毒（Potato virus X，PVX）结果表明，ToLCGdVC 4增强了PVX的致病性，与PVX单独或PVX-mC 4相比，ToLCGdVC 4诱导的植株发育异常更为严重。此外，ToLCGdV C4抑制转基因N.本塞姆氏菌16 c中，但不是由正义GFP诱导的野生型N.本萨米亚那植物此外，C4通过降低16 c-TGS N中35 S启动子的DNA甲基化水平来抑制转录基因沉默（TGS）。本萨米亚那植物此外，C4还可以与受体样激酶（RLK）相互作用，几乎没有MERISTEM 1（BAM 1），这表明C4可以通过干扰BAM 1在RNAi细胞间传播中的功能来抑制基因沉默。这些结果表明C4是ToLCGdV的致病决定因子，C4可能通过与BAM 1相互作用抑制转录后基因沉默（PTGS）。
Tomato leaf curl Guangdong virus (ToLCGdV) is a begomovirus associated with a Tomato yellow leaf curl disease (TYLCD) epidemic in Guangdong province, China. Being the least conserved protein among geminivirus proteins, the function of C4 during ToLCGdV infection has not been elucidated. In this study, the infectious clones of ToLCGdV and a ToLCGdV mutant (ToLCGdVmC4) with disrupted C4 ORF were constructed. Although ToLCGdV and ToLCGdVmC4 could infect Nicotiana benthamiana and tomato plants, ToLCGdVmC4 elicited much milder symptoms compared with ToLCGdV. To further verify the role of C4 in viral pathogenesis, C4 was expressed in N. benthamiana from Potato virus X (PVX) vector. The results showed that ToLCGdV C4 enhanced the pathogenicity of PVX and induced more severe developmental abnormalities in plants compared with PVX alone or PVX-mC4. In addition, ToLCGdV C4 suppresses systemic gene silencing in the transgenic N. benthamiana line 16c, but not local gene silencing induced by sense GFP in wild-type N. benthamiana plants. Moreover, C4 suppresses transcriptional gene silencing (TGS) by reducing the DNA methylation level of 35S promoter in 16c-TGS N. benthamiana plants. Furthermore, C4 could also interact with the receptor-like kinase (RLK) BARELY ANY MERISTEM 1 (BAM1), suggesting that C4 may suppress gene silencing by interfering with the function of BAM1 in the cell-to-cell spread of RNAi. All these results suggest that C4 is a pathogenic determinant of ToLCGdV, and C4 may suppress post-transcriptional gene silencing (PTGS) by interacting with BAM1.