Lettuce chlorosis virus P23 Suppresses RNA Silencing and Induces Local Necrosis with Increased Severity at Raised Temperatures
Lettuce chlorosis virus P23 Suppresses RNA Silencing and Induces Local Necrosis with Increased Severity at Raised Temperatures
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DOI：
10.1094/phyto-09-15-0219-r
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发表时间：
2016-06-01
期刊：
影响因子：
3.2
通讯作者：
Ng, James C. K.
中科院分区：
文献类型：
--
作者：
Kubota, Kenji;Ng, James C. K.
RNA 沉默是植物中的一种抗病毒防御策略，植物病毒通过产生 RNA 沉默的病毒抑制子 (VSR) 来对抗这一策略。已在 Crinivirus 属的三个成员中发现了 VSR，但它们并不都具有相同的抑制机制。在这里，我们使用农杆菌共渗透测定来研究生菜失绿病毒（LCV）编码的蛋白质的抑制活性。在测试抑制野生型本塞姆氏烟草植物中绿色荧光蛋白（GFP）表达沉默的 7 个 LCV 蛋白（1b、P23、HSP70 同源物、P60、CP、CPm 和 P27）中，只有 P23 抑制局部沉默的发生。与 P23 共渗的叶片中小干扰 (si)RNA 积累减少，表明 P23 抑制了 siRNA 的积累或增强了 siRNA 的降解。 P23 还抑制表达 GFP 的转基因本塞姆氏烟草植物中 RNA 沉默的细胞间运动和全身运动。 P23 通过本塞姆氏烟草叶子的农杆菌渗透表达，诱导局部坏死，这种坏死在高温下严重程度增加，这是一个新颖的现象，因为尚未报道其他克里尼病毒 VSR 的温度对坏死严重程度的直接影响。这些结果进一步证实了病毒 VSR 在介导逃避宿主抗病毒防御和症状调节方面的复杂性。
RNA silencing functions as an antivirus defense strategy in plants, one that plant viruses counter by producing viral suppressors of RNA silencing (VSRs). VSRs have been identified in three members of the genus Crinivirus but they do not all share identical suppression mechanisms. Here, we used Agrobacterium co-infiltration assays to investigate the suppressor activity of proteins encoded by Lettuce chlorosis virus (LCV). Of 7 LCV proteins (1b, P23, HSP70 homolog, P60, CP, CPm, and P27) tested for the suppression of silencing of green fluorescent protein (GFP) expression in wild-type Nicotiana benthamiana plants, only P23 suppressed the onset of local silencing. Small-interfering (si)RNA accumulation was reduced in leaves co-infiltrated with P23, suggesting that P23 inhibited the accumulation or enhanced the degradation of siRNA. P23 also inhibited the cell-to-cell and systemic movement of RNA silencing in GFP-expressing transgenic N. benthamiana plants. Expression of P23 via agroinfiltration of N. benthamiana leaves induced local necrosis that increased in severity at elevated temperatures, a novelty given that a direct temperature effect on necrosis severity has not been reported for the other crinivirus VSRs. These results further affirm the sophistication of crinivirus VSRs in mediating the evasion of host's antiviral defenses and in symptom modulation.