Cellular factors involved in transcription and Tax-mediated trans-activation directed by the TGACGT motifs in human T-cell leukemia virus type I promoter.

Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.

Cellular factors involved in transcription and Tax-mediated trans-activation directed by the TGACGT motifs in human T-cell leukemia virus type I promoter.

J Biol Chem. 1990 Nov 25;265(33):20285-92. Unique Identifier : AIDSLINE MED/91056071
Xu YL; Adya N; Siores E; Gao QS; Giam CZ; Department of Biochemistry, University of Nebraska Medical; Center, College of Medicine, Omaha 68198-4525.

Abstract: Human T-cell leukemia virus type I (HTLV-I) encodes a 40-kDa nuclear protein, Tax, which stimulates transcription from three 21-base pair (bp) repeats in its U3 region. Tax trans-activation is mediated via cellular factors that interact with the TGACGT motifs in the 21-bp repeats. Gel mobility shift assay and UV cross-linking analysis show that two proteins of 52 and 46 kDa in size bind the 21-bp repeat specifically. Base substitutions in the TGACGT motif which abolished Tax trans-activation abrogated factor binding whereas the repeats containing mutations that did not affect Tax trans-activation supported factor binding as the wild-type repeat. The 52- and 46-kDa factors are present in human T-cell lines Jurkat and MT4 (HTLV-I transformed) and in HeLa cells but are undetectable in a human placental cell line JEG-3, which gave a reduced level of trans-activation. JEG-3 extracts contain a distinct DNA binding activity that shows analogous sequence requirements as the 52- and 46-kDa proteins in interacting with the various 21-bp repeats. c-Jun and CREB (cAMP-responsive element binding factor) can stimulate transcription from HTLV-I long terminal repeats in JEG-3 cells. At least two copies of the 21-bp repeats are required for optimal trans-activation by c-Jun and CREB. Most single point mutations in the TGACGT motif that abolished Tax trans-activation, however, did not affect c-Jun- or CREB-directed transcriptional enhancement. These data indicate that many transcription factors including c-Jun and CREB exert stimulatory effects on HTLV-I transcription although they do not directly respond to Tax. The 52- and 46-kDa cellular proteins most likely are involved directly in Tax-mediated trans-activation, and they are tentatively named Tax activation factors I and II, respectively.

Keywords: Base Sequence Cell Nucleus/METABOLISM DNA-Binding Proteins/METABOLISM Gene Products, tax/METABOLISM *Genes, pX Hela Cells/METABOLISM Human HTLV-I/*GENETICS Molecular Sequence Data Oligonucleotide Probes Plasmids *Promoter Regions (Genetics) Restriction Mapping Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. *Trans-Activation (Genetics) *Transcription, Genetic JOURNAL ARTICLE
910330
M9130564

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