Transcriptional activation of the human T-lymphotropic virus type I long terminal repeat by functional interaction of Tax1 and Ets1.
AUTOR(ES)
Gitlin, S D
RESUMO
Transcription regulation of the oncogenic retrovirus human T-lymphotropic virus type I (HTLV-I) involves the composite activity of both viral and cellular transcription factors. The HTLV-I transforming protein, Tax1, modulates the activity of several cellular transcription factors, upregulating the level of viral gene expression. In addition, cellular transcription factors, such as Ets1, independently bind to the viral long terminal repeat in a sequence-specific manner and activate transcription. It was of interest to analyze the possible interaction of Tax1 and Ets1 in viral gene regulation. We now report that Tax1 and Ets1 increase expression from the HTLV-I promoter in a cooperative manner. The level of expression was increased 5- to 10-fold above the combined individual effect of Tax1 and Ets1. S1 nuclease analysis demonstrated that the cooperative effect was due to an increase in the levels of steady-state RNA. The functional interaction between Tax1 and Ets1 required the presence of the Tax1-responsive 21-bp repeat element TRE-1 and the Ets1-responsive element ERR-1. These results suggested the possible interaction of Ets1 with transcriptional regulatory proteins that bind to the 21-bp repeats. This interaction is demonstrated by decreased electrophoretic mobility of specific 21-bp repeat gel shift complexes in the presence of Ets1. Furthermore, interaction of Ets1 with the 21-bp repeat-binding proteins enhances the relative efficiency of binding to the DNA. This cooperative interaction between Ets1 and proteins which bind to the Tax1-responsive 21-bp repeats suggests a possible role for Ets1 in the regulation of viral gene expression.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=238194Documentos Relacionados
- Sequence-specific interaction of the Ets1 protein with the long terminal repeat of the human T-lymphotropic virus type I.
- The cellular proto-oncogene product Myb acts as transcriptional activator of the long terminal repeat of human T-lymphotropic virus type I.
- Interaction of the human T-lymphotropic virus type 1 Tax dimer with CREB and the viral 21-base-pair repeat.
- Selective infection of human T-lymphotropic virus type 1 (HTLV-1)-infected cells by chimeric human immunodeficiency viruses containing HTLV-1 tax response elements in the long terminal repeat.
- Serologic confirmation of simian T-lymphotropic virus type I infection by using immunoassays developed for human T-lymphotropic virus antibody detection.