NDLI: The Human T Cell Leukemia/Lymphotropic Virus Type 1 Tax Protein Represses MyoD-dependent Transcription by Inhibiting MyoD-binding to the KIX Domain of p300 A POTENTIAL MECHANISM FOR Tax-MEDIATED REPRESSION OF THE TRANSCRIPTIONAL ACTIVITY OF BASIC HELIX-LOOP-HELIX FACTORS

Content Provider	Journal of Biological Chemistry (JBC)
Author	Riou, Patrice Bex, Françoise Gazzolo, Louis
Abstract	The human T cell leukemia/lymphotropic virus type 1 (HTLV-1) Tax protein strongly activates viral and cellular gene transcription. It mainly functions by interacting with cellular transcription factors and the KIX domain of the p300/CBP coactivators. Tax can also repress the transcription of cellular genes through the basic helix-loop-helix (bHLH) protein family. To investigate the molecular mechanisms of this Tax-mediated inhibition, we analyzed its effect on the transcriptional activity of the myogenic MyoD protein, which was used as a paradigm of bHLH factors. In this study, we show that overexpression of the p300 coactivator in transient transfection assays was sufficient to rescue MyoD repression by Tax. Furthermore, an N-terminal domain of p300 (amino acids 379–654) containing the region of KIX serving as the Tax binding site was found, when overexpressed, to potentiate Tax-mediated transactivation of HTLV-1 proviral as well as MyoD-dependent transcription, and to antagonize the inhibition by Tax of the transcriptional activity of MyoD. These results revealing the presence of an N-terminal MyoD binding site were confirmed by in vitro protein-protein interaction assays that demonstrate that MyoD binds to the KIX domain of p300 and that Tax competes with MyoD binding in a nonreciprocal manner. These observations provide evidence that Tax binding to the KIX domain of p300 prevents bHLH proteins from contacting this N-terminal domain of the coactivator, thus resulting in their transcriptional repression. As bHLH proteins are implicated in many developmental fate decisions, especially during thymopoiesis, Tax-mediated inhibition of their transcriptional activity may contribute to the induction of HTLV-1-linked leukemogenesis.
Related Links	http://www.jbc.org/content/275/14/10551.abstract
Ending Page	10560
Starting Page	10551
Page Count	10
File Format	HTM / HTML PDF
ISSN	00219258
Journal	Journal of Biological Chemistry (JBC)
Issue Number	14
Volume Number	275
DOI	10.1074/jbc.275.14.10551
e-ISSN	1083351X
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2000-04-07
Access Restriction	Open
Subject Keyword	Human T cell leukemia/lymphotropic virus type 1 (HTLV-1) Basic helix-loop-helix (bHLH) Phosphate-buffered saline (PBS) Glutathione S-transferase (GST) Long terminal repeat (LTR) Amino acid(s) (aa) Chloramphenicol acetyltransferase (CAT) Phenylmethylsulfonyl fluoride (PMSF) Dithiothreitol (DTT) Polymerase chain reaction (PCR) Dulbecco's modified Eagle's medium (DMEM) Cyclic AMP response element-binding protein (CREB) Activating transcription factor (ATF) CREB-binding protein (CBP) GENES: STRUCTURE AND REGULATION
Alternative Title	The Human T Cell Leukemia/Lymphotropic Virus Type 1 Tax Protein Represses MyoD-dependent Transcription by Inhibiting MyoD-binding to the KIX Domain of p300
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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