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Nucleic Acids Research, 1989, Vol. 17, No. 13 5207-5222
© 1989

MOLECULAR BIOLOGY

Differential activation of the 21-base-pair enhancer element of human T-cell leukemia virus type 1 by its own trans-activator and cyclic AMP

Masataka Nakamura*, Masaru Niki, Kiyoshi Ohtani and Kazuo Sugamura

Department of Microbiology, Tohoku University School of Medicine Sendai 980, Japan

*To whom correspondance to be addressed

Received April 21, 1989. Revised June 7, 1989. Accepted June 7, 1989.

A transcriptional trans-acting factor ptax of human T-cell leukemia virus type I (HTLV-I) functions as an inducer for expression of HTLV-I provirus via activation of the enhancer in the long terminal repeat of HTLV-I. In addition to p4Otax and a tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C, we report here that forskolin, an activator of adenyl cyclase, also induces function of the HTLV-I enhancer. Experiments with mutants of the HTLV-I enhancer revealed that TPA-induced activation was not mediated by solely a 21-base-pair (bp) sequence that is repeated three times in the enhancer, whereas the 21-bp enhancer element can act as a sufficient cis-acting sequence for activation by both P40tax and forskolin. In addition, we found that nuclear factor(s) like the cyclic AMP-responsive element (CRE) binding factor could bind to the HTLV-I 21-bp enhancer element. However, a difference was found in sequences required for activation by p40tax and forskolin. A CRE related sequence present in the 21-bp enhancer element was enough for forskolin-induced activation. On the other hand, p40tax required a much longer sequence that is overlapping but not identical to the CRE related sequence, suggesting that the forskolin-induced cyclic AMP pathway may be partly involved in, but not sufficient for p40tax-mediating trans-activation of the HTLV-I enhancer.


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