中文摘要：花生芽坏死病毒可引起不同寄主出现坏死症状。先前已有研究表明，活性氧调节的细胞程序性死亡（PCD）会引起坏死症状。病毒蛋白NSs转基因表达可引起病毒症状。本研究通过分析H2O2的积累、抗氧化酶活性以及液泡加工酶的表达水平等揭示了NSs在影响细胞氧化迸发方面的作用。作者根据本研究结果认为，NSs在抑制RNA沉默和诱导细胞死亡中起着双重作用。
外文摘要：Groundnut bud necrosis virus induces necrotic symptoms in different hosts. Previous studies showed reactive oxygen species-mediated programmed cell death (PCD) resulted in necrotic symptoms. Transgenic expression of viral protein NSs mimics viral symptoms. Here, we showed a role for NSs in influencing oxidative burst in the cell, by analyzing H2O2 accumulation, activities of antioxidant enzymes and expression levels of vacuolar processing enzymes, H2O2-responsive microRNA 319a.2 plus its possible target metacaspase-8. The role of NSs in PCD, was shown using two NSs mutants: one in the Trp/GH3 motif (a homologue of pro-apototic domain) (NSs(S189R)) and the other in a non-Trp/GH3 motif (NSs(L172R)). Tobacco rattle virus (TRV) expressing NSs(S189R) enhanced the PCD response, but not TRV-NSs(L172R), while RNA silencing suppression activity was lost in TRV-NSs(L172R), but not in TRV-NSs(S189R). Therefore, we propose dual roles of NSs in RNA silencing suppression and induction of cell death, controlled by different motifs.
外文关键词：MicroRNA; Reaper; Trp/GH3 motif; Vacuolar processing enzyme
作者：Ajeet Singh, Vipin Permar, R.K. Jain，等
作者单位：印度农业研究所
期刊名称：Virology
期刊影响因子：3.47
出版年份：2017
出版刊次：5
点击下载：番茄斑萎病毒属病毒蛋白NSs和模体可诱导细胞死亡但并不能控制RNA沉默抑制活性