State Key Laboratory Breeding Base of Marine Genetic Resources, Key Laboratory of Marine Genetic Resources of State Oceanic Administration, Third Institute of Oceanography, Xiamen, People's Republic of China.
J Virol. 2013 Dec;87(23):12576-82. doi: 10.1128/JVI.01551-13. Epub 2013 Sep 11.
DNA viruses often target cellular proteins to modulate host cell cycles and facilitate viral genome replication. However, whether proliferation of white spot syndrome virus (WSSV) requires regulation of the host cell cycle remains unclear. In the present study, we show that two WSSV paralogs, IE1 and WSV056, can interact with Litopenaeus vannamei retinoblastoma (Rb)-like protein (lv-RBL) through the conserved LxCxE motif. Further investigation revealed that IE1 and WSV056 could also bind to Drosophila retinoblastoma family protein 1 (RBF1) in a manner similar to how they bind to lv-RBL. Using the Drosophila RBF-E2F pathway as a model system, we demonstrated that both IE1 and WSV056 could sequester RBF1 from Drosophila E2F transcription factor 1 (E2F1) and subsequently activate E2F1 to stimulate the G1/S transition. Our findings provide the first evidence that WSSV may regulate cell cycle progression by targeting the Rb-E2F pathway.
DNA 病毒通常靶向细胞蛋白来调节宿主细胞周期并促进病毒基因组复制。然而，白斑综合征病毒（WSSV）的增殖是否需要调节宿主细胞周期尚不清楚。在本研究中，我们表明，两种 WSSV 旁系同源物 IE1 和 WSV056，可以通过保守的 LxCxE 基序与凡纳滨对虾视网膜母细胞瘤（Rb）样蛋白（lv-RBL）相互作用。进一步的研究表明，IE1 和 WSV056 也可以以类似于与 lv-RBL 结合的方式与果蝇视网膜母细胞瘤家族蛋白 1（RBF1）结合。使用果蝇 RBF-E2F 途径作为模型系统，我们证明 IE1 和 WSV056 均可将 RBF1 从果蝇 E2F 转录因子 1（E2F1）中隔离出来，随后激活 E2F1 以刺激 G1/S 期过渡。我们的研究结果首次提供了证据，表明 WSSV 可能通过靶向 Rb-E2F 途径来调节细胞周期进程。
