Braddock M, Thorburn A M, Chambers A, Elliott G D, Anderson G J, Kingsman A J, Kingsman S M
Virus Molecular Biology Group, Department of Biochemistry, Oxford, United Kingdom.
Cell. 1990 Sep 21;62(6):1123-33. doi: 10.1016/0092-8674(90)90389-v.
Replication of HIV-1 depends on the viral Tat protein, which functions via a target sequence, TAR, present in the proviral long terminal repeat (LTR) and at the 5' end of viral mRNAs. We have shown that Tat potentiates the expression of TAR-containing RNAs, but only when Tat and the TAR-containing RNA are present in the nucleus. We now show that a small change in the TAR loop abolishes nuclear potentiation by Tat. Furthermore, the HIV-1 U3 region induces expression incompetence in mRNA synthesized by this promoter. RNAs of identical structure are, however, translated efficiently when produced from the CMV-IE promoter. The Tat-TAR system appears, therefore, to rescue the expression potential of HIV-1 LTR-directed RNA.
