Berkhout B, Gatignol A, Rabson A B, Jeang K T
Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.
Cell. 1990 Aug 24;62(4):757-67. doi: 10.1016/0092-8674(90)90120-4.
Replication of HIV-1 requires Tat, which stimulates gene expression through a target sequence, TAR. It is known that TAR is a Tat-responsive target. Since Tat increases transcriptional initiations from the HIV-1 LTR promoter, it is unclear mechanistically how Tat utilizes an RNA target. Here we show that TAR RNA is only one component of the Tat-responsive target. Efficient Tat trans-activation was observed only when TAR was present in conjunction with the HIV-1 LTR NF-kappa B/SP1 DNA sequences. TAR RNA outside of this context produced a suboptimal Tat response. We propose that TAR RNA serves an attachment function directing Tat to the LTR. A Tat protein engineered to interact with LTR DNA could trans-activate through a TAR-independent mechanism. This suggests that Tat also has a DNA target.
