Replication of a pathogenic non-coding RNA increases DNA methylation in plants associated with a bromodomain-containing viroid-binding protein
文献类型: 外文期刊
作者: Lv, Dian-Qiu 1 ; Liu, Shang-Wu 1 ; Zhao, Jian-Hua 3 ; Zhou, Bang-Jun 3 ; Wang, Shao-Peng 1 ; Guo, Hui-Shan 3 ; Fang, Y 1 ;
作者机构: 1.Heilongjiang Acad Agr Sci, Virus Free Seedling Res Inst, Harbin, Peoples R China
2.Heilongjiang Acad, Agr Sci Postdoctoral Programme, Harbin, Peoples R China
3.Chinese Acad Sci, Inst Microbiol, State Key Lab Plant Genom, Beijing, Peoples R China
4.Univ Nebraska, Plant Sci Innovat Ctr, Lincoln, NE USA
5.Univ Nebraska, Dept Plant Pathol, Lincoln, NE 68583 USA
期刊名称:SCIENTIFIC REPORTS ( 影响因子:4.379; 五年影响因子:5.133 )
ISSN: 2045-2322
年卷期: 2016 年 6 卷
页码:
收录情况: SCI
摘要: Viroids are plant-pathogenic molecules made up of single-stranded circular non-coding RNAs. How replicating viroids interfere with host silencing remains largely unknown. In this study, we investigated the effects of a nuclear-replicating Potato spindle tuber viroid (PSTVd) on interference with plant RNA silencing. Using transient induction of silencing in GFP transgenic Nicotiana benthamiana plants (line 16c), we found that PSTVd replication accelerated GFP silencing and increased Virp1 mRNA, which encodes bromodomain-containing viroid-binding protein 1 and is required for PSTVd replication. DNA methylation was increased in the GFP transgene promoter of PSTVd-replicating plants, indicating involvement of transcriptional gene silencing. Consistently, accelerated GFP silencing and increased DNA methylation in the of GFP transgene promoter were detected in plants transiently expressing Virp1. Virp1 mRNA was also increased upon PSTVd infection in natural host potato plants. Reduced transcript levels of certain endogenous genes were also consistent with increases in DNA methylation in related gene promoters in PSTVd-infected potato plants. Together, our data demonstrate that PSTVd replication interferes with the nuclear silencing pathway in that host plant, and this is at least partially attributable to Virp1. This study provides new insights into the plant-viroid interaction on viroid pathogenicity by subverting the plant cell silencing machinery.
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