College of Plant Protection, Hebei Agricultural University, Baoding, Hebei, 071000, China; State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, 100193, China.
State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, 100193, China.
Virology. 2023 Aug;585:117-126. doi: 10.1016/j.virol.2023.05.011. Epub 2023 Jun 12.
Tomato yellow leaf curl virus (TYLCV) is a monopartite geminivirus, and one of the most devastating plant viruses in the world. TYLCV is traditionally known to encode six viral proteins in bidirectional and partially overlapping open reading frames (ORFs). However, recent studies have shown that TYLCV encodes additional small proteins with specific subcellular localizations and potential virulence functions. Here, a novel protein named C7, encoded by a newly-described ORF in the complementary strand, was identified as part of the TYLCV proteome using mass spectrometry. The C7 protein localized to the nucleus and cytoplasm, both in the absence and presence of the virus. C7 was found to interact with two other TYLCV-encoded proteins: with C2 in the nucleus, and with V2 in the cytoplasm, forming conspicuous granules. Mutation of C7 start codon ATG to ACG to block the translation of C7 delayed the onset of viral infection, and the mutant virus caused milder virus symptoms and less accumulations of viral DNAs and proteins. Using the potato virus X (PVX)-based recombinant vector, we found that ectopic overexpression of C7 resulted in more severe mosaic symptoms and promoted a higher accumulation of PVX-encoded coat protein in the late virus infection stage. In addition, C7 was also found to inhibit GFP-induced RNA silencing moderately. This study demonstrates that the novel C7 protein encoded by TYLCV is a pathogenicity factor and a weak RNA silencing suppressor, and that it plays a critical role during TYLCV infection.
番茄黄曲叶病毒（TYLCV）是一种单分体双生病毒，是世界上最具破坏性的植物病毒之一。TYLCV 传统上被认为在双向和部分重叠的开放阅读框（ORF）中编码六种病毒蛋白。然而，最近的研究表明，TYLCV 编码了具有特定亚细胞定位和潜在毒力功能的额外小蛋白。在这里，一种新型蛋白 C7 被鉴定为 TYLCV 蛋白组的一部分，它是由互补链上新描述的 ORF 编码的。使用质谱法。C7 蛋白定位于细胞核和细胞质中，在没有和存在病毒的情况下都是如此。发现 C7 与 TYLCV 编码的另外两种蛋白相互作用：在细胞核中与 C2 相互作用，在细胞质中与 V2 相互作用，形成明显的颗粒。突变 C7 起始密码子 ATG 为 ACG 以阻止 C7 的翻译会延迟病毒感染的开始，并且突变病毒引起的病毒症状较轻，病毒 DNA 和蛋白质的积累较少。使用马铃薯病毒 X（PVX）为基础的重组载体，我们发现 C7 的异位过表达导致更严重的花叶症状，并在后期病毒感染阶段促进更高水平的 PVX 编码外壳蛋白的积累。此外，还发现 C7 适度抑制 GFP 诱导的 RNA 沉默。这项研究表明，TYLCV 编码的新型 C7 蛋白是一种致病性因子和弱 RNA 沉默抑制剂，它在 TYLCV 感染过程中起着关键作用。
