Response of the human T-cell leukemia virus type 1 long terminal repeat to cyclic AMP.
The sequences that control transcriptional initiation of the provirus of the human T-cell leukemia virus type 1 (HTLV-1) are shown to be responsive to intracellular levels of cyclic AMP. A heptanucleotide sequence present within the 21-nucleotide repeat sequence that is similar to the cyclic AMP-responsive consensus (CRE) sequence was required for cyclic AMP-mediated increase in gene expression. Although the CRE-like sequences were contained within sequences that were responsive to the virally encoded trans-activator (tax), the evidence presented indicates that the mechanisms of promoter induction by the tax product and cyclic AMP are independent. The implication of cyclic AMP stimulation of HTLV-1 provirus gene expression for long-term persistence of infected T cells and for virus-induced transformation is discussed.
Poteat
H T
HT
Department of Cancer Biology, Harvard School of Public Health, Boston, Massachusetts.
Kadison
P
P
McGuire
K
K
Park
L
L
Park
R E
RE
Sodroski
J G
JG
Haseltine
W A
WA
D002460:Cell Line; D000242:Cyclic AMP / Q000494:pharmacology*; D005786:Gene Expression Regulation; D015486:HTLV-I Antigens / Q000502:physiology; D015368:Human T-lymphotropic virus 1 / Q000235:genetics*; D006801:Humans; D012045:Regulatory Sequences, Nucleic Acid; D012091:Repetitive Sequences, Nucleic Acid; D012191:Retroviridae Proteins / Q000235:genetics*; D015534:Trans-Activators; D014157:Transcription Factors / Q000235:genetics / Q000502:physiology
D015486:HTLV-I Antigens; D012191:Retroviridae Proteins; D015534:Trans-Activators; D014157:Transcription Factors; D000242:Cyclic AMP