Journal of Virology, January 1999, p. 738-745, Vol. 73, No. 1
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Department of Molecular Biology,
Received 10 August 1998/Accepted 12 October 1998
The Tax transactivator protein of human T-cell leukemia virus type
1 (HTLV-1) plays a central role in the activation of viral gene
expression. In addition, Tax is capable of activating the expression of
specific cellular genes and is involved in the transformation of
T-lymphocytes resulting in the development of adult T-cell leukemia. Tax is a phosphoprotein that colocalizes in nuclear bodies with RNA polymerase II, splicing complexes, and specific transcription factors including members of the ATF/CREB and NF-
B families. In this study, we identified adjacent serine residues at
positions 300 and 301 in the carboxy terminus of Tax as the major sites
for phosphorylation. Phosphorylation of at least one of these serine
residues is required for Tax localization in nuclear bodies and for
Tax-mediated activation of gene expression via both the ATF/CREB and
NF-
B pathways. Introduction of amino acid substitutions which are
phosphoserine mimetics at positions 300 and 301 restored the ability of
a phosphorylation-defective Tax mutant to form nuclear bodies and to
activate gene expression. These studies define sites for regulatory
phosphorylation events in Tax which are critical for its ability to
activate gene transcription.
*
Corresponding author. Mailing address:
Département de Biologie Moléculaire, Université Libre
de Bruxelles, 67, Rue des Chevaux, B-1640 Rhode St Genèse,
Belgium. Phone: 32 2 6509825. Fax: 32 2 6509839. E-mail:
fbex{at}dbm.ulb.ac.be.
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