Document 0592 DOCN M9550592 TI Definition of a minimal activation domain in human T-cell leukemia virus type I Tax. DT 9505 AU Semmes OJ; Jeang KT; Molecular Virology Section, National Institute of Allergy and; Infectious Diseases, Bethesda, Maryland 20892. SO J Virol. 1995 Mar;69(3):1827-33. Unique Identifier : AIDSLINE MED/95156615 AB Fourteen mutants were used to delineate a minimal activation domain in the Tax protein of human T-cell leukemia virus type I. In an assay using a Gal4-Tax (GalTx) fusion protein and a responsive promoter containing Gal4 consensus binding sites, we found that activation was squelched by coexpression of wild-type Tax protein in trans. When Tax mutants were tested for squelching, many competed effectively against GalTx. However, those containing changes in amino acids 289 to 322 failed to inhibit activity. In particular, three mutants that were expressed stably, with changes at amino acids 289, 296, and 320 respectively, did not squelch GalTx activity. On the other hand, mutants with individual changes at amino acid 3, 9, 29, 41, 273, and 337 efficiently inhibited GalTx function. Three other mutants failed to be stably expressed. In separate experiments, when fused alone to the DNA-binding domain of Gal4, amino acids 289 to 322 of Tax conferred trans activation ability. This fusion protein was able to activate a core promoter. These findings suggest that amino acids 289 to 322 define a region that contacts an essential transcription factor and that this region is a modular activation domain. DE Amino Acid Sequence Binding Sites Chimeric Proteins Consensus Sequence Gene Expression Regulation, Viral Gene Products, tax/*CHEMISTRY/METABOLISM HTLV-I/*GENETICS Molecular Sequence Data Sequence Deletion Structure-Activity Relationship Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. *Trans-Activation (Genetics) Transcription Factors/METABOLISM JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).