Activation of NF-kappa B by the HTLV-I trans-activator protein Tax requires an additional factor present in lymphoid cells.
The Tax protein of human T-cell leukemia virus is a potent transcriptional activator of viral and cellular genes, including the genes for interleukin 2 and interleukin 2 receptor alpha chain (IL2R alpha). The NF-kappa B protein has been implicated in Tax-mediated activation of IL2R alpha gene expression. We show that activation of NF-kappa B by Tax is an indirect process that requires prior activation of a preexistent factor that is present in lymphoid cells. Deletion mutagenesis revealed that the carboxyl-terminal acidic region of Tax is required for activation of IL2R alpha-directed gene expression but dispensable for activation of the long terminal repeat (LTR). Our findings suggest that activation of viral and cellular gene expression by Tax is achieved through a cascade of events that involves multiple protein-protein associations and that the specificity of these associations is conferred through different domains of the Tax protein.
Ruben
S M
SM
Department of Molecular Oncology and Virology, Roche Research Center, Nutley, NJ 07110.
Perkins
A
A
Rosen
C A
CA
D001402:B-Lymphocytes / Q000276:immunology; D001483:Base Sequence; D002460:Cell Line; D004247:DNA / Q000235:genetics; D005786:Gene Expression Regulation; D016356:Gene Products, tax / Q000235:genetics*; D015368:Human T-lymphotropic virus 1 / Q000235:genetics*; D006801:Humans; D008969:Molecular Sequence Data; D009154:Mutation; D016328:NF-kappa B / Q000235:genetics*; D015375:Receptors, Interleukin-2 / Q000235:genetics
D016356:Gene Products, tax; D016328:NF-kappa B; D015375:Receptors, Interleukin-2; D004247:DNA