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Transcription Factor Binding and Histone Modifications on the Integrated Proviral Promoter in Human T-cell Leukemia Virus-I-infected T-cells
The human T-cell leukemia virus (HTLV-I)-encoded Tax protein is a potent transcriptional activator that stimulates expression of the integrated provirus. Biochemical studies indicate that Tax, together with cellular transcription factors, interacts with viral cAMP-response element enhancer elements...
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| Published in: | The Journal of biological chemistry 2002-12, Vol.277 (51), p.49459-49465 |
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| container_end_page | 49465 |
| container_issue | 51 |
| container_start_page | 49459 |
| container_title | The Journal of biological chemistry |
| container_volume | 277 |
| creator | Lemasson, Isabelle Polakowski, Nicholas J. Laybourn, Paul J. Nyborg, Jennifer K. |
| description | The human T-cell leukemia virus (HTLV-I)-encoded Tax protein is a potent transcriptional activator that stimulates expression of the integrated provirus. Biochemical studies indicate that Tax, together with cellular transcription factors, interacts with viral cAMP-response element enhancer elements to recruit the pleiotropic coactivators CREB-binding protein and p300. Histone acetylation by these coactivators has been shown to play a major role in activating HTLV-I transcription from chromatin templates in vitro. However, the extent of histone modification and the precise identity of the cellular regulatory proteins bound at the HTLV-I promoter in vivo is not known. Chromatin immunoprecipitation analysis was used to investigate factor binding and histone modification at the integrated HTLV-I provirus in infected T-cells (SLB-1). These studies reveal the presence of Tax, a variety of ATF/CREB and AP-1 family members (CREB, CREB-2, ATF-1, ATF-2, c-Fos, and c-Jun), and both p300 and CREB-binding protein at the HTLV-I promoter. Consistent with the binding of these coactivators, we observed histone H3 and H4 acetylation at three regions within the proviral genome. Histone deacetylases were also present at the viral promoter and, following their inhibition, we observe an increase in histone H4 acetylation on the HTLV-I promoter and a concomitant increase in viral RNA. Together, these results suggest that a variety of transcriptional activators, coactivators, and histone deacetylases participate in the regulation of HTLV-I transcription in infected T-cells. |
| doi_str_mv | 10.1074/jbc.M209566200 |
| format | article |
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Biochemical studies indicate that Tax, together with cellular transcription factors, interacts with viral cAMP-response element enhancer elements to recruit the pleiotropic coactivators CREB-binding protein and p300. Histone acetylation by these coactivators has been shown to play a major role in activating HTLV-I transcription from chromatin templates in vitro. However, the extent of histone modification and the precise identity of the cellular regulatory proteins bound at the HTLV-I promoter in vivo is not known. Chromatin immunoprecipitation analysis was used to investigate factor binding and histone modification at the integrated HTLV-I provirus in infected T-cells (SLB-1). These studies reveal the presence of Tax, a variety of ATF/CREB and AP-1 family members (CREB, CREB-2, ATF-1, ATF-2, c-Fos, and c-Jun), and both p300 and CREB-binding protein at the HTLV-I promoter. Consistent with the binding of these coactivators, we observed histone H3 and H4 acetylation at three regions within the proviral genome. Histone deacetylases were also present at the viral promoter and, following their inhibition, we observe an increase in histone H4 acetylation on the HTLV-I promoter and a concomitant increase in viral RNA. Together, these results suggest that a variety of transcriptional activators, coactivators, and histone deacetylases participate in the regulation of HTLV-I transcription in infected T-cells.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M209566200</identifier><identifier>PMID: 12386157</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acetylation ; Chromatin - metabolism ; Cyclic AMP - metabolism ; Genes, Viral ; Histones - metabolism ; Human T-lymphotropic virus 1 - metabolism ; Humans ; Models, Genetic ; Nuclear Proteins - metabolism ; Plasmids - metabolism ; Polymerase Chain Reaction ; Precipitin Tests ; Promoter Regions, Genetic ; Protein Binding ; Protein Structure, Tertiary ; Single-Strand Specific DNA and RNA Endonucleases - metabolism ; T-Lymphocytes - virology ; Trans-Activators - metabolism ; Transcription Factor AP-1 - metabolism ; Transcription Factors - metabolism ; Transcription, Genetic</subject><ispartof>The Journal of biological chemistry, 2002-12, Vol.277 (51), p.49459-49465</ispartof><rights>2002 © 2002 ASBMB. 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Biochemical studies indicate that Tax, together with cellular transcription factors, interacts with viral cAMP-response element enhancer elements to recruit the pleiotropic coactivators CREB-binding protein and p300. Histone acetylation by these coactivators has been shown to play a major role in activating HTLV-I transcription from chromatin templates in vitro. However, the extent of histone modification and the precise identity of the cellular regulatory proteins bound at the HTLV-I promoter in vivo is not known. Chromatin immunoprecipitation analysis was used to investigate factor binding and histone modification at the integrated HTLV-I provirus in infected T-cells (SLB-1). These studies reveal the presence of Tax, a variety of ATF/CREB and AP-1 family members (CREB, CREB-2, ATF-1, ATF-2, c-Fos, and c-Jun), and both p300 and CREB-binding protein at the HTLV-I promoter. Consistent with the binding of these coactivators, we observed histone H3 and H4 acetylation at three regions within the proviral genome. Histone deacetylases were also present at the viral promoter and, following their inhibition, we observe an increase in histone H4 acetylation on the HTLV-I promoter and a concomitant increase in viral RNA. Together, these results suggest that a variety of transcriptional activators, coactivators, and histone deacetylases participate in the regulation of HTLV-I transcription in infected T-cells.</description><subject>Acetylation</subject><subject>Chromatin - metabolism</subject><subject>Cyclic AMP - metabolism</subject><subject>Genes, Viral</subject><subject>Histones - metabolism</subject><subject>Human T-lymphotropic virus 1 - metabolism</subject><subject>Humans</subject><subject>Models, Genetic</subject><subject>Nuclear Proteins - metabolism</subject><subject>Plasmids - metabolism</subject><subject>Polymerase Chain Reaction</subject><subject>Precipitin Tests</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Binding</subject><subject>Protein Structure, Tertiary</subject><subject>Single-Strand Specific DNA and RNA Endonucleases - metabolism</subject><subject>T-Lymphocytes - virology</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Transcription Factors - metabolism</subject><subject>Transcription, Genetic</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNqF0UGPEyEYBmBiNG539erRcDDepgIDw8xRN7u2STd6qMYbYeCblrUDFZg1_gd_9DJpkz0ZucDheb984UXoDSVLSiT_cN-b5R0jnWgaRsgztKCkrata0B_P0YIQRquOifYCXaZ0T8rhHX2JLiir24YKuUB_t1H7ZKI7Zhc8vtUmh4g_OW-d32HtLV65lIMHfBesG5zRs0u42LwHvPYZdlFnsPhrDA8u6sP8GEOGiJ3Hq2nUHm8rA4cD3sD0E0an8XcXp1StK-cHMHP2BNIr9GLQhwSvz_cV-nZ7s71eVZsvn9fXHzeV4ZzkahiA2VYI20naCyPBaqMbwxnjnayNbaktrukptURK1jet4IaTnkGRlIn6Cr0_zT3G8GuClNXo0ryB9hCmpCSTjRQd-y-kbcPqRtAClydoYkgpwqCO0Y06_lGUqLkoVYpST0WVwNvz5KkfwT7xczMFvDuBvdvtf7sIqnfB7GFUTEolqOIdF11h7YlB-a8HB1El48AbsCVisrLB_WuFR-dqrrs</recordid><startdate>20021220</startdate><enddate>20021220</enddate><creator>Lemasson, Isabelle</creator><creator>Polakowski, Nicholas J.</creator><creator>Laybourn, Paul J.</creator><creator>Nyborg, Jennifer K.</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20021220</creationdate><title>Transcription Factor Binding and Histone Modifications on the Integrated Proviral Promoter in Human T-cell Leukemia Virus-I-infected T-cells</title><author>Lemasson, Isabelle ; 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Consistent with the binding of these coactivators, we observed histone H3 and H4 acetylation at three regions within the proviral genome. Histone deacetylases were also present at the viral promoter and, following their inhibition, we observe an increase in histone H4 acetylation on the HTLV-I promoter and a concomitant increase in viral RNA. Together, these results suggest that a variety of transcriptional activators, coactivators, and histone deacetylases participate in the regulation of HTLV-I transcription in infected T-cells.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12386157</pmid><doi>10.1074/jbc.M209566200</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acetylation Chromatin - metabolism Cyclic AMP - metabolism Genes, Viral Histones - metabolism Human T-lymphotropic virus 1 - metabolism Humans Models, Genetic Nuclear Proteins - metabolism Plasmids - metabolism Polymerase Chain Reaction Precipitin Tests Promoter Regions, Genetic Protein Binding Protein Structure, Tertiary Single-Strand Specific DNA and RNA Endonucleases - metabolism T-Lymphocytes - virology Trans-Activators - metabolism Transcription Factor AP-1 - metabolism Transcription Factors - metabolism Transcription, Genetic |
| title | Transcription Factor Binding and Histone Modifications on the Integrated Proviral Promoter in Human T-cell Leukemia Virus-I-infected T-cells |
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