中文摘要：由于RNA沉默，顶端分生组织（SAM）对大多数植物病毒具有抗性。如果RNA沉默受到病毒RNA沉默抑制因子（VSRs）的抑制时，就会促进病毒对SAM的瞬时侵入。在许多情况下，会出现慢性症状和长期病毒恢复的现象，但其潜在的机制知之甚少。本文研究发现，虽然野生黄瓜花叶病毒（CMVWT）短暂地侵入了SAM，但随后就被从分生组织中剔除。出乎意料地是，一个CMV突变体会持久地侵入SAM，从而导致顶端优势明显降低。值得注意的是，在感染病毒的植株新叶片中，CMVWT病毒诱导出的抗病毒沉默比CMVRA强。研究结果表明，CMV外壳蛋白是调节抗病毒沉默和VSRs活性的中央枢纽，并可介导病毒的自衰减和长期症状的恢复。
外文摘要：Shoot apical meristems (SAM) are resistant to most plant viruses due to RNA silencing, which is restrained by viral suppressors of RNA silencing (VSRs) to facilitate transient viral invasion of the SAM. In many cases chronic symptoms and long-term virus recovery occur, but the underlying mechanisms are poorly understood. Here, we found that wild-type Cucumber mosaic virus (CMVWT) invaded the SAM transiently, but was subsequently eliminated from the meristems. Unexpectedly, a CMV mutant, designated CMVRA that harbors an alanine substitution in the N-terminal arginine-rich region of the coat protein (CP) persistently invaded the SAM and resulted in visible reductions in apical dominance. Notably, the CMVWT virus elicited more potent antiviral silencing than CMVRA in newly emerging leaves of infected plants. However, both viruses caused severe symptoms with minimal antiviral silencing effects in the Arabidopsis mutants lacking host RNA-DEPENDENT RNA POLYMERASE 6 (RDR6) or SUPPRESSOR OF GENE SILENCING 3 (SGS3), indicating that CMVWT induced host RDR6/SGS3-dependent antiviral silencing. We also showed that reduced accumulation of the 2b protein is elicited in the CMVWT infection and consequently rescues potent antiviral RNA silencing. Indeed, co-infiltration assays showed that the suppression of posttranscriptional gene silencing mediated by 2b is more severely compromised by co-expression of CPWT than by CPRA. We further demonstrated that CPWT had high RNA binding activity leading to translation inhibition in wheat germ systems, and CPWT was associated with SGS3 into punctate granules in vivo. Thus, we propose that the RNAs bound and protected by CPWT possibly serve as templates of RDR6/SGS3 complexes for siRNA amplification. Together, these findings suggest that the CMV CP acts as a central hub that modulates antiviral silencing and VSRs activity, and mediates viral self-attenuation and long-term symptom recovery.
作者：Zhang, Xiao-Peng; Liu, De-Shui; Yan, Teng; 等
作者单位：中国农业大学
期刊名称：PLOS PATHOGENS
期刊影响因子：6.608
出版年份：2017
出版刊次：7
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