Repression of turnip crinkle virus replication by its replication protein p88
Repression of turnip crinkle virus replication by its replication protein p88
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DOI：
10.1016/j.virol.2018.10.024
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发表时间：
2019-01-02
期刊：
影响因子：
3.7
通讯作者：
Qu, Feng
中科院分区：
文献类型：
--
作者：
Zhang, Shaoyan;Sun, Rong;Qu, Feng
我们最近报道了两种芜菁皱纹病毒(TCV)复制蛋白之一p28反式互补了缺失p28的TCV，但抑制了另一种编码野生型p28的TCV复制子的复制(Zhang等，2017)。在这里，我们显示了P88，TCV编码的RNA依赖的RNA聚合酶，同样反式互补了P88缺陷的TCV复制子，但抑制了编码野生型P88的复制子。令人惊讶的是，降低P88蛋白水平增强了反式互补作用，但削弱了抑制作用。P88的抑制不仅仅是由于蛋白质的过度表达，因为缺失127或224个N末端氨基酸的缺失突变体积累到更高的水平，但都是较差的阻遏因子。最后，P88的反式互补和抑制都伴随着亚基因组RNA2的优先积累和一类新的小TCV RNAs。我们的结果表明，P88对TCV复制的抑制可能表现为一种病毒机制，即根据P88的丰度来调节基因组和亚基因组RNA的比例。
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.