Genomic androgen receptor-occupied regions with different functions, defined by histone acetylation, coregulators and transcriptional capacity
The androgen receptor (AR) is a steroid-activated transcription factor that binds at specific DNA locations and plays a key role in the etiology of prostate cancer. While numerous studies have identified a clear connection between AR binding and expression of target genes for a limited number of loc...
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| description | The androgen receptor (AR) is a steroid-activated transcription factor that binds at specific DNA locations and plays a key role in the etiology of prostate cancer. While numerous studies have identified a clear connection between AR binding and expression of target genes for a limited number of loci, high-throughput elucidation of these sites allows for a deeper understanding of the complexities of this process.
We have mapped 189 AR occupied regions (ARORs) and 1,388 histone H3 acetylation (AcH3) loci to a 3% continuous stretch of human genomic DNA using chromatin immunoprecipitation (ChIP) microarray analysis. Of 62 highly reproducible ARORs, 32 (52%) were also marked by AcH3. While the number of ARORs detected in prostate cancer cells exceeded the number of nearby DHT-responsive genes, the AcH3 mark defined a subclass of ARORs much more highly associated with such genes -- 12% of the genes flanking AcH3+ARORs were DHT-responsive, compared to only 1% of genes flanking AcH3-ARORs. Most ARORs contained enhancer activities as detected in luciferase reporter assays. Analysis of the AROR sequences, followed by site-directed ChIP, identified binding sites for AR transcriptional coregulators FoxA1, CEBPbeta, NFI and GATA2, which had diverse effects on endogenous AR target gene expression levels in siRNA knockout experiments.
We suggest that only some ARORs function under the given physiological conditions, utilizing diverse mechanisms. This diversity points to differential regulation of gene expression by the same transcription factor related to the chromatin structure. |
| doi_str_mv | 10.1371/journal.pone.0003645 |
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We have mapped 189 AR occupied regions (ARORs) and 1,388 histone H3 acetylation (AcH3) loci to a 3% continuous stretch of human genomic DNA using chromatin immunoprecipitation (ChIP) microarray analysis. Of 62 highly reproducible ARORs, 32 (52%) were also marked by AcH3. While the number of ARORs detected in prostate cancer cells exceeded the number of nearby DHT-responsive genes, the AcH3 mark defined a subclass of ARORs much more highly associated with such genes -- 12% of the genes flanking AcH3+ARORs were DHT-responsive, compared to only 1% of genes flanking AcH3-ARORs. Most ARORs contained enhancer activities as detected in luciferase reporter assays. Analysis of the AROR sequences, followed by site-directed ChIP, identified binding sites for AR transcriptional coregulators FoxA1, CEBPbeta, NFI and GATA2, which had diverse effects on endogenous AR target gene expression levels in siRNA knockout experiments.
We suggest that only some ARORs function under the given physiological conditions, utilizing diverse mechanisms. This diversity points to differential regulation of gene expression by the same transcription factor related to the chromatin structure.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0003645</identifier><identifier>PMID: 18997859</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acetates ; Acetylation ; Analysis ; Androgen receptors ; Androgens ; B cells ; Binding sites ; Biochemistry/Transcription and Translation ; Cancer ; Cell Line, Tumor ; Chromatin ; Chromatin Immunoprecipitation ; Chromosomes, Human, Pair 19 - genetics ; Chromosomes, Human, Pair 20 - genetics ; Deoxyribonucleic acid ; Development and progression ; DNA ; DNA microarrays ; Epigenetics ; Etiology ; Gene expression ; Genes ; Genetic aspects ; Genetics and Genomics ; Genome, Human ; Histone H3 ; Histones - metabolism ; Humans ; Immunoprecipitation ; Loci ; Male ; Models, Biological ; Molecular Biology/Chromatin Structure ; Molecular Biology/Histone Modification ; Nuclear factor I ; Physiological aspects ; Prostate cancer ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Receptors, Androgen - genetics ; Receptors, Androgen - metabolism ; Response Elements - genetics ; siRNA ; Transcription (Genetics) ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transcription, Genetic</subject><ispartof>PloS one, 2008-11, Vol.3 (11), p.e3645-e3645</ispartof><rights>COPYRIGHT 2008 Public Library of Science</rights><rights>2008 Jia et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Jia et al. 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c662t-6e02161efec68ccbbb32733cd717959c477f9b11d8ee89fde66ba4fc59e5ff9f3</citedby><cites>FETCH-LOGICAL-c662t-6e02161efec68ccbbb32733cd717959c477f9b11d8ee89fde66ba4fc59e5ff9f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577007/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577007/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18997859$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jia, Li</creatorcontrib><creatorcontrib>Berman, Benjamin P</creatorcontrib><creatorcontrib>Jariwala, Unnati</creatorcontrib><creatorcontrib>Yan, Xiting</creatorcontrib><creatorcontrib>Cogan, Jon P</creatorcontrib><creatorcontrib>Walters, Allison</creatorcontrib><creatorcontrib>Chen, Ting</creatorcontrib><creatorcontrib>Buchanan, Grant</creatorcontrib><creatorcontrib>Frenkel, Baruch</creatorcontrib><creatorcontrib>Coetzee, Gerhard A</creatorcontrib><title>Genomic androgen receptor-occupied regions with different functions, defined by histone acetylation, coregulators and transcriptional capacity</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The androgen receptor (AR) is a steroid-activated transcription factor that binds at specific DNA locations and plays a key role in the etiology of prostate cancer. While numerous studies have identified a clear connection between AR binding and expression of target genes for a limited number of loci, high-throughput elucidation of these sites allows for a deeper understanding of the complexities of this process.
We have mapped 189 AR occupied regions (ARORs) and 1,388 histone H3 acetylation (AcH3) loci to a 3% continuous stretch of human genomic DNA using chromatin immunoprecipitation (ChIP) microarray analysis. Of 62 highly reproducible ARORs, 32 (52%) were also marked by AcH3. While the number of ARORs detected in prostate cancer cells exceeded the number of nearby DHT-responsive genes, the AcH3 mark defined a subclass of ARORs much more highly associated with such genes -- 12% of the genes flanking AcH3+ARORs were DHT-responsive, compared to only 1% of genes flanking AcH3-ARORs. Most ARORs contained enhancer activities as detected in luciferase reporter assays. Analysis of the AROR sequences, followed by site-directed ChIP, identified binding sites for AR transcriptional coregulators FoxA1, CEBPbeta, NFI and GATA2, which had diverse effects on endogenous AR target gene expression levels in siRNA knockout experiments.
We suggest that only some ARORs function under the given physiological conditions, utilizing diverse mechanisms. This diversity points to differential regulation of gene expression by the same transcription factor related to the chromatin structure.</description><subject>Acetates</subject><subject>Acetylation</subject><subject>Analysis</subject><subject>Androgen receptors</subject><subject>Androgens</subject><subject>B cells</subject><subject>Binding sites</subject><subject>Biochemistry/Transcription and Translation</subject><subject>Cancer</subject><subject>Cell Line, Tumor</subject><subject>Chromatin</subject><subject>Chromatin Immunoprecipitation</subject><subject>Chromosomes, Human, Pair 19 - genetics</subject><subject>Chromosomes, Human, Pair 20 - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>DNA</subject><subject>DNA microarrays</subject><subject>Epigenetics</subject><subject>Etiology</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetics and Genomics</subject><subject>Genome, Human</subject><subject>Histone H3</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Loci</subject><subject>Male</subject><subject>Models, Biological</subject><subject>Molecular Biology/Chromatin Structure</subject><subject>Molecular Biology/Histone Modification</subject><subject>Nuclear factor I</subject><subject>Physiological aspects</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Receptors, Androgen - genetics</subject><subject>Receptors, Androgen - metabolism</subject><subject>Response Elements - genetics</subject><subject>siRNA</subject><subject>Transcription (Genetics)</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transcription, Genetic</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk9-L1DAQx4so3nn6H4gWhAPhdk2aNmlehOPQc-HgwF-vIU0mu1m6SU1Sdf8J_2bT21V3xQfpQ5qZz3wnmcwUxVOM5pgw_Grtx-BkPx-8gzlCiNC6uVecYk6qGa0QuX_wf1I8inGNUENaSh8WJ7jlnLUNPy1-XIPzG6tK6XTwS3BlAAVD8mHmlRoHCzpblta7WH6zaVVqawwEcKk0o1NpclyUGox1mey25crGlE9USgVp28sJuCiVzxpj3vkQp0xlCtJFFeww-WVfKjlIZdP2cfHAyD7Ck_16Vnx6--bj1bvZze314uryZqYordKMAqowxWBA0VaprutIxQhRmmHGG65qxgzvMNYtQMuNBko7WRvVcGiM4YacFc93ukPvo9iXMgpMcEUwoYRkYrEjtJdrMQS7kWErvLTizuDDUsiQrOpBEJ5FcxLdIlqDQbLltSYNb2oNnNST1ut9trHbgFa5ekH2R6LHHmdXYum_iqphDCGWBc73AsF_GSEmsbFRQd9LB36MgnJGOcFNBl_8Bf77bvMdtZT5-NYZn7Oq_GnIrZBfz9hsv6xZ1VDG2zYHvDwKyEyC72kpxxjF4sP7_2dvPx-z5wfsCmSfVtH3411bHYP1DlTBxxjA_C4eRmIah1_3FNM4iP045LBnh4X_E7Tvf_ITMu4LaA</recordid><startdate>20081110</startdate><enddate>20081110</enddate><creator>Jia, Li</creator><creator>Berman, Benjamin P</creator><creator>Jariwala, Unnati</creator><creator>Yan, Xiting</creator><creator>Cogan, Jon P</creator><creator>Walters, Allison</creator><creator>Chen, Ting</creator><creator>Buchanan, Grant</creator><creator>Frenkel, Baruch</creator><creator>Coetzee, Gerhard A</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20081110</creationdate><title>Genomic androgen receptor-occupied regions with different functions, defined by histone acetylation, coregulators and transcriptional capacity</title><author>Jia, Li ; Berman, Benjamin P ; Jariwala, Unnati ; Yan, Xiting ; Cogan, Jon P ; Walters, Allison ; Chen, Ting ; Buchanan, Grant ; Frenkel, Baruch ; Coetzee, Gerhard A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c662t-6e02161efec68ccbbb32733cd717959c477f9b11d8ee89fde66ba4fc59e5ff9f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Acetates</topic><topic>Acetylation</topic><topic>Analysis</topic><topic>Androgen receptors</topic><topic>Androgens</topic><topic>B cells</topic><topic>Binding sites</topic><topic>Biochemistry/Transcription and Translation</topic><topic>Cancer</topic><topic>Cell Line, Tumor</topic><topic>Chromatin</topic><topic>Chromatin Immunoprecipitation</topic><topic>Chromosomes, Human, Pair 19 - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jia, Li</au><au>Berman, Benjamin P</au><au>Jariwala, Unnati</au><au>Yan, Xiting</au><au>Cogan, Jon P</au><au>Walters, Allison</au><au>Chen, Ting</au><au>Buchanan, Grant</au><au>Frenkel, Baruch</au><au>Coetzee, Gerhard A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genomic androgen receptor-occupied regions with different functions, defined by histone acetylation, coregulators and transcriptional capacity</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2008-11-10</date><risdate>2008</risdate><volume>3</volume><issue>11</issue><spage>e3645</spage><epage>e3645</epage><pages>e3645-e3645</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The androgen receptor (AR) is a steroid-activated transcription factor that binds at specific DNA locations and plays a key role in the etiology of prostate cancer. While numerous studies have identified a clear connection between AR binding and expression of target genes for a limited number of loci, high-throughput elucidation of these sites allows for a deeper understanding of the complexities of this process.
We have mapped 189 AR occupied regions (ARORs) and 1,388 histone H3 acetylation (AcH3) loci to a 3% continuous stretch of human genomic DNA using chromatin immunoprecipitation (ChIP) microarray analysis. Of 62 highly reproducible ARORs, 32 (52%) were also marked by AcH3. While the number of ARORs detected in prostate cancer cells exceeded the number of nearby DHT-responsive genes, the AcH3 mark defined a subclass of ARORs much more highly associated with such genes -- 12% of the genes flanking AcH3+ARORs were DHT-responsive, compared to only 1% of genes flanking AcH3-ARORs. Most ARORs contained enhancer activities as detected in luciferase reporter assays. Analysis of the AROR sequences, followed by site-directed ChIP, identified binding sites for AR transcriptional coregulators FoxA1, CEBPbeta, NFI and GATA2, which had diverse effects on endogenous AR target gene expression levels in siRNA knockout experiments.
We suggest that only some ARORs function under the given physiological conditions, utilizing diverse mechanisms. This diversity points to differential regulation of gene expression by the same transcription factor related to the chromatin structure.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>18997859</pmid><doi>10.1371/journal.pone.0003645</doi><tpages>e3645</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2008-11, Vol.3 (11), p.e3645-e3645 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1312313633 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Acetates Acetylation Analysis Androgen receptors Androgens B cells Binding sites Biochemistry/Transcription and Translation Cancer Cell Line, Tumor Chromatin Chromatin Immunoprecipitation Chromosomes, Human, Pair 19 - genetics Chromosomes, Human, Pair 20 - genetics Deoxyribonucleic acid Development and progression DNA DNA microarrays Epigenetics Etiology Gene expression Genes Genetic aspects Genetics and Genomics Genome, Human Histone H3 Histones - metabolism Humans Immunoprecipitation Loci Male Models, Biological Molecular Biology/Chromatin Structure Molecular Biology/Histone Modification Nuclear factor I Physiological aspects Prostate cancer Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Receptors, Androgen - genetics Receptors, Androgen - metabolism Response Elements - genetics siRNA Transcription (Genetics) Transcription Factors - genetics Transcription Factors - metabolism Transcription, Genetic |
| title | Genomic androgen receptor-occupied regions with different functions, defined by histone acetylation, coregulators and transcriptional capacity |
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