Knutson Bruce A, Oh Jaewook, Broyles Steven S
Department of Biochemistry, Purdue University, West Lafayette, IN 47907, USA.
J Gen Virol. 2009 Jul;90(Pt 7):1592-1599. doi: 10.1099/vir.0.006924-0. Epub 2009 Mar 18.
Approximately half of the intermediate and late gene transcriptional promoters of vaccinia virus have a binding site for the cellular transcription factor YY1 that overlaps the initiator elements. Depletion of YY1 using RNA interference enhanced the activity of these promoters, while overexpression of YY1 repressed their activity. Viral promoter nucleotide replacements that specifically impair the binding of YY1 mostly alleviated the transcriptional repression and correlated with the ability of YY1 to stably interact with the initiator DNAs in vitro. The transcriptional repression activity was localized to the C-terminal DNA-binding domain of the protein. These results indicate that YY1 functions to negatively regulate these vaccinia virus promoters by binding to their initiator elements.
痘苗病毒的大约一半的中晚期基因转录启动子具有与起始元件重叠的细胞转录因子YY1的结合位点。使用RNA干扰使YY1耗竭可增强这些启动子的活性,而YY1的过表达则抑制其活性。特异性损害YY1结合的病毒启动子核苷酸替换大多缓解了转录抑制,并与YY1在体外与起始DNA稳定相互作用的能力相关。转录抑制活性定位于该蛋白的C末端DNA结合结构域。这些结果表明,YY1通过与其起始元件结合来负向调节这些痘苗病毒启动子。