Singh Ajeet, Permar Vipin, Jain R K, Goswami Suneha, Kumar Ranjeet Ranjan, Canto Tomas, Palukaitis Peter, Praveen Shelly
Division of Biochemistry, Indian Agricultural Research Institute, New Delhi 110012, India.
Division of Plant Pathology, Indian Agricultural Research Institute, New Delhi 110012, India.
Virology. 2017 Aug;508:108-117. doi: 10.1016/j.virol.2017.05.003. Epub 2017 May 17.
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 HO accumulation, activities of antioxidant enzymes and expression levels of vacuolar processing enzymes, HO-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) and the other in a non-Trp/GH3 motif (NSs). Tobacco rattle virus (TRV) expressing NSs enhanced the PCD response, but not TRV-NSs, while RNA silencing suppression activity was lost in TRV-NSs, but not in TRV-NSs. Therefore, we propose dual roles of NSs in RNA silencing suppression and induction of cell death, controlled by different motifs.
花生芽坏死病毒在不同宿主中引发坏死症状。先前的研究表明，活性氧介导的程序性细胞死亡（PCD）导致了坏死症状。病毒蛋白NSs的转基因表达模拟了病毒症状。在此，我们通过分析过氧化氢（HO）积累、抗氧化酶活性、液泡加工酶的表达水平、HO响应性微小RNA 319a.2及其可能的靶标metacaspase-8，揭示了NSs在影响细胞氧化爆发中的作用。使用两个NSs突变体展示了NSs在PCD中的作用：一个在Trp/GH3基序（促凋亡结构域的同源物）中（NSs），另一个在非Trp/GH3基序中（NSs）。表达NSs的烟草脆裂病毒（TRV）增强了PCD反应，但TRV-NSs没有，而TRV-NSs丧失了RNA沉默抑制活性，但TRV-NSs没有。因此，我们提出NSs在RNA沉默抑制和细胞死亡诱导中具有双重作用，这由不同的基序控制。
