Posttranscriptional gene silencing (PTGS) is one of the most important mechanisms for plants during viral infection. However, viruses have also developed viral suppressors to negatively control PTGS by inhibiting microRNA (miRNA) and short-interfering RNA (siRNA) regulation in plants. The first identified viral suppressor, P1/HC-Pro, is a fusion protein that was translated from potyviral RNA. Upon infecting plants, the P1 protein itself is released from HC-Pro by the self-cleaving activity of P1. P1 has an unknown function in enhancing HC-Pro-mediated PTGS suppression. We performed proteomics to identify P1-interacting proteins. We also performed transcriptomics that were generated from Col-0 and various P1/HC-Pro-related transgenic plants to identify novel genes. The results showed several novel genes were identified through the comparative network analysis that might be involved in P1/HC-Pro-mediated PTGS suppression. First, we demonstrated that P1 enhances HC-Pro function and that the mechanism might work through P1 binding to VERNALIZATION INDEPENDENCE 3/SUPERKILLER 8 (VIP3/SKI8), a subunit of the exosome, to interfere with the 5′-fragment of the PTGS-cleaved RNA degradation product. Second, the AGO1 was specifically posttranslationally degraded in transgenic Arabidopsis expressing P1/HC-Pro of turnip mosaic virus (TuMV) (P1/HCTu plant). Third, the comparative network highlighted potentially critical genes in PTGS, including miRNA targets, calcium signaling, hormone (JA, ET, and ABA) signaling, and defense response. Through these genetic and omics approaches, we revealed an overall perspective to identify many critical genes involved in PTGS. These new findings significantly impact in our understanding of P1/HC-Pro-mediated PTGS suppression.

中文翻译：

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通过遗传学和组学方法研究P1对HC-pro介导的基因沉默抑制的影响。

转录后基因沉默（PTGS）是植物在病毒感染过程中最重要的机制之一。但是，病毒还开发了病毒抑制剂，通过抑制植物中的microRNA（miRNA）和短干扰RNA（siRNA）来负向控制PTGS。最早鉴定出的病毒抑制物P1 / HC-Pro是一种融合蛋白，是从马铃薯病毒RNA中翻译出来的。感染植物后，P1蛋白本身会通过P1的自我切割活性而从HC-Pro中释放出来。P1在增强HC-Pro介导的PTGS抑制中具有未知功能。我们进行了蛋白质组学鉴定与P1相互作用的蛋白质。我们还进行了从Col-0和各种P1 / HC-Pro相关转基因植物中生成的转录组学，以鉴定新基因。结果表明，通过比较网络分析鉴定出了一些可能与P1 / HC-Pro介导的PTGS抑制有关的新基因。首先，我们证明了P1增强了HC-Pro功能，并且该机制可能通过P1与外泌体的一个亚基VERNALIZATION INDEPENDENCE 3 / SUPERKILLER 8（VIP3 / SKI8）结合而起作用，以干扰PTGS的5'片段-切割的RNA降解产物。第二，AGO1在表达萝卜花叶病毒P1 / HC-Pro（TuMV）（P1 / HCTu植物）的P1 / HC-Pro的转基因拟南芥中被特异地翻译后降解。第三，比较网络强调了PTGS中潜在的关键基因，包括miRNA靶标，钙信号传导，激素（JA，ET和ABA）信号传导和防御反应。通过这些基因组学方法，我们揭示了一个整体观点，以鉴定参与PTGS的许多关键基因。这些新发现极大地影响了我们对P1 / HC-Pro介导的PTGS抑制的理解。