Journal
VIROLOGY
Volume 324, Issue 2, Pages 540-553Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2004.04.008
Keywords
HTLV-1; LTR; SRF; SRE; basal transcription; T cell activation; latency
Categories
Funding
- NCI NIH HHS [T32 CA 09197, CA 55684] Funding Source: Medline
- NIAID NIH HHS [T32 AI 07471] Funding Source: Medline
Ask authors/readers for more resources
In response to various mitogenic signals, serum response factor (SRF) activates cellular gene expression after binding to its cognate target sequence (CArG box) located within a serum response element (SRE). SRF is particularly important in T cell activation, and we now report that SIZE activates basal transcription from the human T-cell leukemia virus-1 (HTLV-1) long terminal repeat (LTR). A DNA element, with similarity to the consensus cellular CArG box found in the c-fos promoter centered approximately 120 base pairs upstream from the viral transcription start site, has been identified and named the vCArG box. SRF activation of gene expression from the LTR was localized to the vCArG box, and mutation of this site abolished SRF responsiveness. An oligonucleotide probe containing the vCArG box bound purified SRF, and a complex formed on this probe with nuclear extract was supershifted by anti-SRF antibody. Moreover, a biotinylated probe containing the vCArG box bound SRF in avidin-biotin pull-down assays. Quantitative binding analysis yielded nanomolar affinities for both the viral and cellular CArG boxes. Chromatin immunoprecipitation experiments demonstrated that SRF is resident on the HTLV-1 LTR in vivo. These data identify a functional serum response element in the HTLV-1 LTR and suggest that SRF may play an important role in regulating basal HTLV-1 gene expression in early infection and reactivation from latency. (C) 2004 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available