Induction of the HTLV-I LTR by Jun occurs through the Tax-responsive 21-bp elements.

The HTLV-I LTR is known to be induced by a variety of cellular signals. Tax protein is one potent viral trans-activator of LTR-directed transcription. We demonstrate here that Jun is another transcription factor that can strongly modulate the activity of this LTR. Using deletion and competition studies, the minimal portion of the LTR for Jun activation was found to coincide with the Tax-responsive 21-bp elements. In binding experiments, nuclear factors that bound to the HTLV-I 21-bp sequence were competed by an excess of AP-1 motif oligonucleotide. Although the Tax-responsive elements do not contain a strictly conserved AP-1 motif, these findings suggest that they function as AP-1 sites. We found, however, that in cells depleted for AP-1 activity (F9 teratocarcinoma), Tax activation of the HTLV-I LTR was maintained. Thus while Jun/AP-1 may be involved in the basal expression of the HTLV-I LTR, it may not be essential for Tax-mediated activation.