中文摘要：水稻黑条矮缩病毒（RBSDV）是引起玉米粗缩病的常见病原，在中国常会造成严重减产。然而，RBSDV与玉米之间的交互作用很大程度上是未知的。RNA沉默是植物抗病毒的一种保守机制。为了理解感染RBSDV植物中抗病毒RNA干扰反应，本研究通过深度测序技术获得来自玉米病株中RBSDV的病毒衍生小干扰RNAs（vsiRNAs）图谱。本研究结果表明，RBSDV衍生的siRNAs优先分布在几个基因组片段的5'- 或3'- 末端区域。此外，研究结果还表明，在RBSDV侵染过程中抗病毒RNA沉默途径中涉及到的有些成分的mRNA水平呈差异性表达。
外文摘要：Rice black streaked dwarf virus (RBSDV) is the casual agent of maize rough dwarf disease, which frequently causes severe yield loss in China. However, the interaction between RBSDV and maize plants is largely unknown. RNA silencing is a conserved mechanism against viruses in plants. To understand the antiviral RNA interfering response in RBSDV-infected plants, the profile of virus-derived small interfering RNAs (vsiRNAs) from RBSDV in infected maize plants was obtained by deep sequencing in this study. Our data showed that vsiRNAs, accumulated preferentially as 21- and 22-nucleotide (nt) species, were mapped against all 10 genomic RNA segments of RBSDV and derived almost equally overall from both positive and negative strands, while there were significant differences in the accumulation level of vsiRNAs from segments 2,4, 6, 7 and 10. The vsiRNAs (21 and 22 nt) generated from each segment of RBSDV genome had a 5'-terminal nucleotide bias toward adenine and uracil. The single-nucleotide resolution maps showed that RBSDV-derived siRNAs preferentially distributed in the 5'- or 3'-terminal regions of several genomic segments. In addition, our results showed that the mRNA levels of some components involved in antiviral RNA silencing pathway were differentially modified during RBSDV infection. Among them, the accumulation levels of ZinDCL1, ZmDCL2,ZmDCL3a,ZmAGO1a, ZmAGO1b, ZmAGO2a, ZmAG018a and ZmRDR6 mRNAs were significantly up-regulated, while those of ZmDCL3b, ZmDCL4 and ZmAGO1c mRNAs showed no obvious changes in RBSDV-infected maize plants.
外文关键词：Fijivirus; Rice black streaked dwarf virus; Virus-derived small interfering RNA; Deep sequencing; RNA silencing
作者：Li, Mingjun; Li, Yongqiang; Xia, Zihao; 等
作者单位：中国农业大学
期刊名称：VIRUS RESEARCH
期刊影响因子：2.526
出版年份：2017
出版刊次：1
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