The transcription elongation factor ELL2 is specifically upregulated in HTLV-1-infected T-cells and is dependent on the viral oncoprotein Tax

Abstract The oncoprotein Tax of human T-cell leukemia virus type 1 (HTLV-1) is a potent transactivator of viral and cellular transcription. Here, we identified ELL2 as the sole transcription elongation factor to be specifically upregulated in HTLV-1-/Tax-transformed T-cells. Tax contributes to regul...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2014-09, Vol.464, p.98-110
Main Authors: Mann, Melanie C, Strobel, Sarah, Fleckenstein, Bernhard, Kress, Andrea K
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
ELL2
ELONGATION
Gene Expression Regulation, Viral
Gene Products, tax - genetics
Gene Products, tax - metabolism
GENE REGULATION
HTLV-1
HTLV-I Infections - genetics
HTLV-I Infections - metabolism
HTLV-I Infections - virology
Human T-cell leukemia virus type 1
Human T-lymphotropic virus 1 - genetics
Human T-lymphotropic virus 1 - metabolism
Humans
IN VIVO
Infectious Disease
LEUKEMIA VIRUSES
LYMPHOCYTES
MESSENGER-RNA
Promoter Regions, Genetic
PROMOTERS
T-Lymphocytes - metabolism
T-Lymphocytes - virology
Tax
TRANSCRIPTION
Transcription elongation factor
Transcriptional Activation
Transcriptional Elongation Factors - genetics
Transcriptional Elongation Factors - metabolism
Up-Regulation
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Summary:Abstract The oncoprotein Tax of human T-cell leukemia virus type 1 (HTLV-1) is a potent transactivator of viral and cellular transcription. Here, we identified ELL2 as the sole transcription elongation factor to be specifically upregulated in HTLV-1-/Tax-transformed T-cells. Tax contributes to regulation of ELL2, since transient transfection of Tax increases ELL2 mRNA, Tax transactivates the ELL2 promoter, and repression of Tax results in decrease of ELL2 in transformed T-lymphocytes. However, we also measured upregulation of ELL2 in HTLV-1-transformed cells exhibiting undetectable amounts of Tax , suggesting that ELL2 can still be maintained independent of continuous Tax expression. We further show that Tax and ELL2 synergistically activate the HTLV-1 promoter, indicating that ELL2 cooperates with Tax in viral transactivation. This is supported by our findings that Tax and ELL2 accumulate in nuclear fractions and that they co-precipitate upon co-expression in transiently-transfected cells. Thus, upregulation of ELL2 could contribute to HTLV-1 gene regulation.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2014.06.028