Department of Plant Pathology, The Ohio State University, Wooster, OH 44691, USA.
Department of Plant Pathology, The Ohio State University, Wooster, OH 44691, USA; Fujian Key Laboratory of Plant Virology, Institute of Plant Virology, Fujian Agriculture and Forestry University, Fuzhou, China.
Virology. 2019 Jan 2;526:165-172. doi: 10.1016/j.virol.2018.10.024. Epub 2018 Nov 2.
We recently reported that p28, one of the two turnip crinkle virus (TCV) replication proteins, trans-complemented a defective TCV lacking p28, yet repressed the replication of another TCV replicon encoding wild-type p28 (Zhang et al., 2017). Here we show that p88, the TCV-encoded RNA-dependent RNA polymerase, likewise trans-complemented a p88-defective TCV replicon, but repressed one encoding wild-type p88. Surprisingly, lowering p88 protein levels enhanced trans-complementation, but weakened repression. Repression by p88 was not simply due to protein over-expression, as deletion mutants missing 127 or 224 N-terminal amino acids accumulated to higher levels but were poor repressors. Finally, both trans-complementation and repression by p88 were accompanied by preferential accumulation of subgenomic RNA2, and a novel class of small TCV RNAs. Our results suggest that repression of TCV replication by p88 may manifest a viral mechanism that regulates the ratio of genomic and subgenomic RNAs based on p88 abundance.
我们最近报道称,芜菁黄花叶病毒(TCV)的两种复制蛋白之一 p28 可转互补缺乏 p28 的缺陷型 TCV,但会抑制另一种编码野生型 p28 的 TCV 复制子的复制(Zhang 等人,2017)。在这里,我们发现 TCV 编码的 RNA 依赖性 RNA 聚合酶 p88 同样可以转互补 p88 缺陷型 TCV 复制子,但会抑制编码野生型 p88 的复制子。令人惊讶的是,降低 p88 蛋白水平会增强转互补作用,但会削弱抑制作用。p88 的抑制作用并非仅仅由于蛋白过表达所致,因为缺失 127 或 224 个 N 端氨基酸的缺失突变体积累到更高水平,但抑制作用较差。最后,p88 的转互补和抑制作用都伴随着亚基因组 RNA2 和一类新的 TCV 小 RNA 的优先积累。我们的结果表明,p88 对 TCV 复制的抑制作用可能表现出一种病毒机制,根据 p88 丰度调节基因组和亚基因组 RNA 的比例。