Guo Liu-Ming, Li Jing, Qi Pan-Pan, Qing Ling, Zhang Heng-Mu
Laboratory of Virology, Innovation Center of Chinese Medicine Crops, Institute of Virology and Biotechnology, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China; Chongqing Key Laboratory of Plant Disease Biology, College of Plant Protection, Southwest University, Chongqing 400716, China.
Laboratory of Virology, Innovation Center of Chinese Medicine Crops, Institute of Virology and Biotechnology, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China.
Plant Commun. 2025 Aug 11;6(8):101413. doi: 10.1016/j.xplc.2025.101413. Epub 2025 Jun 10.
Geminiviruses are widespread across the globe and cause devastating diseases in food and medicinal crops. Their C3 proteins have long been known to enhance viral replication; however, the underlying molecular mechanisms remain poorly understood. In this study, we show that transgenic plants overexpressing the C3 protein of tobacco curly shoot geminivirus (TbCSV) exhibit hypersensitive responses to cytokinin (CK) treatment, which largely restores the attenuated viral replication observed in the TbCSV C3 mutant (TbCSV). We identified NbTAF12b, a negative regulator of CK signaling in Nicotiana benthamiana, as a C3-interacting protein that attenuates TbCSV replication. TbCSV C3 not only inhibits the transcription of NbTAF12b but also competes with NbRR1 and NbKMD17 for binding to the NbTAF12b protein. This competition disrupts the formation of the NbTAF12b-NbKMD-NbRR heterotrimer and promotes NbRR1 accumulation, thereby enhancing CK signaling and ultimately facilitating TbCSV replication. C3 proteins from other distantly related geminiviruses exhibit similar 3D structures and also target NbTAF12b in vivo, suggesting that this mechanism is conserved among geminiviruses. These findings shed new light on the molecular mechanism by which TbCSV C3 facilitates viral replication through the modulation of CK signaling and provide potential molecular targets for engineering virus-resistant plants.
双生病毒在全球广泛分布，可导致粮食作物和药用作物发生毁灭性病害。长期以来，人们已知其C3蛋白可增强病毒复制；然而，其潜在的分子机制仍知之甚少。在本研究中，我们发现过表达烟草曲茎双生病毒（TbCSV）C3蛋白的转基因植物对细胞分裂素（CK）处理表现出超敏反应，这在很大程度上恢复了在TbCSV C3突变体（TbCSV）中观察到的减弱的病毒复制。我们鉴定出本氏烟草中CK信号的负调控因子NbTAF12b是一种与C3相互作用的蛋白，可减弱TbCSV复制。TbCSV C3不仅抑制NbTAF12b的转录，还与NbRR1和NbKMD17竞争结合NbTAF12b蛋白。这种竞争破坏了NbTAF12b-NbKMD-NbRR异源三聚体的形成，并促进NbRR1积累，从而增强CK信号，最终促进TbCSV复制。来自其他远缘双生病毒的C3蛋白表现出相似的三维结构，并且在体内也靶向NbTAF12b，这表明该机制在双生病毒中是保守的。这些发现为TbCSV C3通过调节CK信号促进病毒复制的分子机制提供了新的见解，并为培育抗病毒植物提供了潜在的分子靶点。
