Recruitment of cyclin T1/P-TEFb to an HIV type 1 long terminal repeat promoter proximal RNA target is both necessary and sufficient for full activation of transcription

摘要: Transcriptional activation of the HIV type 1 (HIV-1) long terminal repeat (LTR) promoter element by viral Tat protein is an essential step in HIV-1 life cycle. function mediated TAR RNA target encoded within LTR and known to require recruitment a complex consisting cyclin T1 (CycT1) component positive transcription elongation factor b (P-TEFb) TAR. Here, we demonstrate that both become entirely dispensable for when CycT1/P-TEFb artificially recruited heterologous proximal target. The level observed was indistinguishable from induced neither inhibited nor increased expressed trans. Activation CycT1 depended on ability bind CDK9 P-TEFb. In contrast, although binding act as cofactor, these interactions became directly LTR. Importantly, found be at elongation. Together, data fully sufficient activate this imply sole role Tat/TAR axis permit CycT1/P-TEFb.