Role of PU.1 in MHC Class II Expression via CIITA Transcription in Plasmacytoid Dendritic Cells
The cofactor CIITA is a master regulator of MHC class II expression and several transcription factors regulating the cell type-specific expression of CIITA have been identified. Although the MHC class II expression in plasmacytoid dendritic cells (pDCs) is also mediated by CIITA, the transcription f...
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| creator | Miura, Ryosuke Kasakura, Kazumi Nakano, Nobuhiro Hara, Mutsuko Maeda, Keiko Okumura, Ko Ogawa, Hideoki Yashiro, Takuya Nishiyama, Chiharu |
| description | The cofactor CIITA is a master regulator of MHC class II expression and several transcription factors regulating the cell type-specific expression of CIITA have been identified. Although the MHC class II expression in plasmacytoid dendritic cells (pDCs) is also mediated by CIITA, the transcription factors involved in the CIITA expression in pDCs are largely unknown. In the present study, we analyzed the role of a hematopoietic lineage-specific transcription factor, PU.1, in CIITA transcription in pDCs. The introduction of PU.1 siRNA into mouse pDCs and a human pDC cell line, CAL-1, reduced the mRNA levels of MHC class II and CIITA. When the binding of PU.1 to the 3rd promoter of CIITA (pIII) in CAL-1 and mouse pDCs was analyzed by a chromatin immunoprecipitation assay, a significant amount of PU.1 binding to the pIII was detected, which was definitely decreased in PU.1 siRNA-transfected cells. Reporter assays showed that PU.1 knockdown reduced the pIII promoter activity and that three Ets-motifs in the human pIII promoter were candidates of cis-enhancing elements. By electrophoretic mobility shift assays, it was confirmed that two Ets-motifs, GGAA (-181/-178) and AGAA (-114/-111), among three candidates, were directly bound with PU.1. When mouse pDCs and CAL-1 cells were stimulated by GM-CSF, mRNA levels of PU.1, pIII-driven CIITA, total CIITA, MHC class II, and the amount of PU.1 binding to pIII were significantly increased. The GM-CSF-mediated up-regulation of these mRNAs was canceled in PU.1 siRNA-introduced cells. Taking these results together, we conclude that PU.1 transactivates the pIII through direct binding to Ets-motifs in the promoter in pDCs. |
| doi_str_mv | 10.1371/journal.pone.0154094 |
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Although the MHC class II expression in plasmacytoid dendritic cells (pDCs) is also mediated by CIITA, the transcription factors involved in the CIITA expression in pDCs are largely unknown. In the present study, we analyzed the role of a hematopoietic lineage-specific transcription factor, PU.1, in CIITA transcription in pDCs. The introduction of PU.1 siRNA into mouse pDCs and a human pDC cell line, CAL-1, reduced the mRNA levels of MHC class II and CIITA. When the binding of PU.1 to the 3rd promoter of CIITA (pIII) in CAL-1 and mouse pDCs was analyzed by a chromatin immunoprecipitation assay, a significant amount of PU.1 binding to the pIII was detected, which was definitely decreased in PU.1 siRNA-transfected cells. Reporter assays showed that PU.1 knockdown reduced the pIII promoter activity and that three Ets-motifs in the human pIII promoter were candidates of cis-enhancing elements. By electrophoretic mobility shift assays, it was confirmed that two Ets-motifs, GGAA (-181/-178) and AGAA (-114/-111), among three candidates, were directly bound with PU.1. When mouse pDCs and CAL-1 cells were stimulated by GM-CSF, mRNA levels of PU.1, pIII-driven CIITA, total CIITA, MHC class II, and the amount of PU.1 binding to pIII were significantly increased. The GM-CSF-mediated up-regulation of these mRNAs was canceled in PU.1 siRNA-introduced cells. Taking these results together, we conclude that PU.1 transactivates the pIII through direct binding to Ets-motifs in the promoter in pDCs.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0154094</identifier><identifier>PMID: 27105023</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Antigens ; Assaying ; Binding ; Biology and life sciences ; Bone marrow ; Cell Line ; Chromatin ; CIITA protein ; Dendritic cells ; Dendritic Cells - immunology ; Electrophoretic mobility ; ETS protein ; Gene expression ; Gene Knockdown Techniques ; Genetic aspects ; Granulocyte-macrophage colony-stimulating factor ; Histocompatibility Antigens Class II - immunology ; Humans ; Immunology ; Immunoprecipitation ; Laboratories ; Lymphocytes ; Major histocompatibility complex ; Medicine ; Medicine and Health Sciences ; Mice ; Mice, Inbred BALB C ; Molecular biology ; Nuclear Proteins - genetics ; Penicillin ; Physiological aspects ; Promoter Regions, Genetic ; Protein Binding ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - physiology ; PU.1 protein ; Research and Analysis Methods ; RNA, Small Interfering - genetics ; Rodents ; Science ; siRNA ; T cell receptors ; Trans-Activators - genetics ; Trans-Activators - physiology ; Transcription factors ; Transcription, Genetic</subject><ispartof>PloS one, 2016-04, Vol.11 (4), p.e0154094-e0154094</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Miura et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (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>2016 Miura et al 2016 Miura et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c791t-aabcbbbe1f9be8007bcfd3e453618f1b9fbbc3ba7c4b68e11e39af20c9cd53423</citedby><cites>FETCH-LOGICAL-c791t-aabcbbbe1f9be8007bcfd3e453618f1b9fbbc3ba7c4b68e11e39af20c9cd53423</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/PMC4841550/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841550/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23864,27922,27923,53789,53791,79370,79371</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27105023$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Sadegh-Nasseri, Scheherazade</contributor><creatorcontrib>Miura, Ryosuke</creatorcontrib><creatorcontrib>Kasakura, Kazumi</creatorcontrib><creatorcontrib>Nakano, Nobuhiro</creatorcontrib><creatorcontrib>Hara, Mutsuko</creatorcontrib><creatorcontrib>Maeda, Keiko</creatorcontrib><creatorcontrib>Okumura, Ko</creatorcontrib><creatorcontrib>Ogawa, Hideoki</creatorcontrib><creatorcontrib>Yashiro, Takuya</creatorcontrib><creatorcontrib>Nishiyama, Chiharu</creatorcontrib><title>Role of PU.1 in MHC Class II Expression via CIITA Transcription in Plasmacytoid Dendritic Cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The cofactor CIITA is a master regulator of MHC class II expression and several transcription factors regulating the cell type-specific expression of CIITA have been identified. Although the MHC class II expression in plasmacytoid dendritic cells (pDCs) is also mediated by CIITA, the transcription factors involved in the CIITA expression in pDCs are largely unknown. In the present study, we analyzed the role of a hematopoietic lineage-specific transcription factor, PU.1, in CIITA transcription in pDCs. The introduction of PU.1 siRNA into mouse pDCs and a human pDC cell line, CAL-1, reduced the mRNA levels of MHC class II and CIITA. When the binding of PU.1 to the 3rd promoter of CIITA (pIII) in CAL-1 and mouse pDCs was analyzed by a chromatin immunoprecipitation assay, a significant amount of PU.1 binding to the pIII was detected, which was definitely decreased in PU.1 siRNA-transfected cells. Reporter assays showed that PU.1 knockdown reduced the pIII promoter activity and that three Ets-motifs in the human pIII promoter were candidates of cis-enhancing elements. By electrophoretic mobility shift assays, it was confirmed that two Ets-motifs, GGAA (-181/-178) and AGAA (-114/-111), among three candidates, were directly bound with PU.1. When mouse pDCs and CAL-1 cells were stimulated by GM-CSF, mRNA levels of PU.1, pIII-driven CIITA, total CIITA, MHC class II, and the amount of PU.1 binding to pIII were significantly increased. The GM-CSF-mediated up-regulation of these mRNAs was canceled in PU.1 siRNA-introduced cells. Taking these results together, we conclude that PU.1 transactivates the pIII through direct binding to Ets-motifs in the promoter in pDCs.</description><subject>Analysis</subject><subject>Animals</subject><subject>Antigens</subject><subject>Assaying</subject><subject>Binding</subject><subject>Biology and life sciences</subject><subject>Bone marrow</subject><subject>Cell Line</subject><subject>Chromatin</subject><subject>CIITA protein</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - immunology</subject><subject>Electrophoretic mobility</subject><subject>ETS protein</subject><subject>Gene expression</subject><subject>Gene Knockdown Techniques</subject><subject>Genetic aspects</subject><subject>Granulocyte-macrophage colony-stimulating factor</subject><subject>Histocompatibility Antigens Class II - immunology</subject><subject>Humans</subject><subject>Immunology</subject><subject>Immunoprecipitation</subject><subject>Laboratories</subject><subject>Lymphocytes</subject><subject>Major histocompatibility complex</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Molecular biology</subject><subject>Nuclear Proteins - genetics</subject><subject>Penicillin</subject><subject>Physiological aspects</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Binding</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>PU.1 protein</subject><subject>Research and Analysis Methods</subject><subject>RNA, Small Interfering - genetics</subject><subject>Rodents</subject><subject>Science</subject><subject>siRNA</subject><subject>T cell receptors</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - physiology</subject><subject>Transcription factors</subject><subject>Transcription, Genetic</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk19v0zAUxSMEYmPwDRBYQkLw0GLHzh-_IFVhsEhDm0bHq3XtOK2rNC52Mm3fHodmU4P2MOXB0fXvnNwc-0bRW4LnhGbky8b2roVmvrOtnmOSMMzZs-iYcBrP0hjT5wfvR9Er7zcYJzRP05fRUZwRnOCYHkfiyjYa2RpdXs8JMi36eVagogHvUVmi09ud094b26IbA6goy-UCLR20Xjmz64Z6kFwGfAvqrrOmQt90WznTGYUK3TT-dfSihsbrN-N6El1_P10WZ7Pzix9lsTifqYyTbgYglZRSk5pLnWOcSVVXVLOEpiSvieS1lIpKyBSTaa4J0ZRDHWPFVZVQFtOT6P3ed9dYL8ZsvCBZTtNssAlEuScqCxuxc2YL7k5YMOJfwbqVABf6brSAWAMBHmdMAcsZQMpixrOqSkkqgePg9XX8Wi-3ulK67Rw0E9PpTmvWYmVvRHAjSTIYfBoNnP3Ta9-JrfEqBAattv3QN2eMJzzmT0BzxlJK4iSgH_5DHw9ipFYQ_tW0tQ0tqsFULNgQZppmg9f8ESo8ld4aFe5cbUJ9Ivg8EQSm07fdCnrvRfnr6unsxe8p-_GAXWtourW3TT_cPj8F2R5UznrvdP1wHgSLYWTu0xDDyIhxZILs3eFZPojuZ4T-BQgND1w</recordid><startdate>20160422</startdate><enddate>20160422</enddate><creator>Miura, Ryosuke</creator><creator>Kasakura, Kazumi</creator><creator>Nakano, Nobuhiro</creator><creator>Hara, Mutsuko</creator><creator>Maeda, Keiko</creator><creator>Okumura, Ko</creator><creator>Ogawa, Hideoki</creator><creator>Yashiro, Takuya</creator><creator>Nishiyama, Chiharu</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>20160422</creationdate><title>Role of PU.1 in MHC Class II Expression via CIITA Transcription in Plasmacytoid Dendritic Cells</title><author>Miura, Ryosuke ; Kasakura, Kazumi ; Nakano, Nobuhiro ; Hara, Mutsuko ; Maeda, Keiko ; Okumura, Ko ; Ogawa, Hideoki ; Yashiro, Takuya ; Nishiyama, Chiharu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c791t-aabcbbbe1f9be8007bcfd3e453618f1b9fbbc3ba7c4b68e11e39af20c9cd53423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Antigens</topic><topic>Assaying</topic><topic>Binding</topic><topic>Biology and life sciences</topic><topic>Bone marrow</topic><topic>Cell Line</topic><topic>Chromatin</topic><topic>CIITA protein</topic><topic>Dendritic cells</topic><topic>Dendritic Cells - 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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>Miura, Ryosuke</au><au>Kasakura, Kazumi</au><au>Nakano, Nobuhiro</au><au>Hara, Mutsuko</au><au>Maeda, Keiko</au><au>Okumura, Ko</au><au>Ogawa, Hideoki</au><au>Yashiro, Takuya</au><au>Nishiyama, Chiharu</au><au>Sadegh-Nasseri, Scheherazade</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of PU.1 in MHC Class II Expression via CIITA Transcription in Plasmacytoid Dendritic Cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-04-22</date><risdate>2016</risdate><volume>11</volume><issue>4</issue><spage>e0154094</spage><epage>e0154094</epage><pages>e0154094-e0154094</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The cofactor CIITA is a master regulator of MHC class II expression and several transcription factors regulating the cell type-specific expression of CIITA have been identified. Although the MHC class II expression in plasmacytoid dendritic cells (pDCs) is also mediated by CIITA, the transcription factors involved in the CIITA expression in pDCs are largely unknown. In the present study, we analyzed the role of a hematopoietic lineage-specific transcription factor, PU.1, in CIITA transcription in pDCs. The introduction of PU.1 siRNA into mouse pDCs and a human pDC cell line, CAL-1, reduced the mRNA levels of MHC class II and CIITA. When the binding of PU.1 to the 3rd promoter of CIITA (pIII) in CAL-1 and mouse pDCs was analyzed by a chromatin immunoprecipitation assay, a significant amount of PU.1 binding to the pIII was detected, which was definitely decreased in PU.1 siRNA-transfected cells. Reporter assays showed that PU.1 knockdown reduced the pIII promoter activity and that three Ets-motifs in the human pIII promoter were candidates of cis-enhancing elements. By electrophoretic mobility shift assays, it was confirmed that two Ets-motifs, GGAA (-181/-178) and AGAA (-114/-111), among three candidates, were directly bound with PU.1. When mouse pDCs and CAL-1 cells were stimulated by GM-CSF, mRNA levels of PU.1, pIII-driven CIITA, total CIITA, MHC class II, and the amount of PU.1 binding to pIII were significantly increased. The GM-CSF-mediated up-regulation of these mRNAs was canceled in PU.1 siRNA-introduced cells. Taking these results together, we conclude that PU.1 transactivates the pIII through direct binding to Ets-motifs in the promoter in pDCs.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27105023</pmid><doi>10.1371/journal.pone.0154094</doi><tpages>e0154094</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1783674536 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Analysis Animals Antigens Assaying Binding Biology and life sciences Bone marrow Cell Line Chromatin CIITA protein Dendritic cells Dendritic Cells - immunology Electrophoretic mobility ETS protein Gene expression Gene Knockdown Techniques Genetic aspects Granulocyte-macrophage colony-stimulating factor Histocompatibility Antigens Class II - immunology Humans Immunology Immunoprecipitation Laboratories Lymphocytes Major histocompatibility complex Medicine Medicine and Health Sciences Mice Mice, Inbred BALB C Molecular biology Nuclear Proteins - genetics Penicillin Physiological aspects Promoter Regions, Genetic Protein Binding Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - physiology PU.1 protein Research and Analysis Methods RNA, Small Interfering - genetics Rodents Science siRNA T cell receptors Trans-Activators - genetics Trans-Activators - physiology Transcription factors Transcription, Genetic |
| title | Role of PU.1 in MHC Class II Expression via CIITA Transcription in Plasmacytoid Dendritic Cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-09T17%3A03%3A30IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Role%20of%20PU.1%20in%20MHC%20Class%20II%20Expression%20via%20CIITA%20Transcription%20in%20Plasmacytoid%20Dendritic%20Cells&rft.jtitle=PloS%20one&rft.au=Miura,%20Ryosuke&rft.date=2016-04-22&rft.volume=11&rft.issue=4&rft.spage=e0154094&rft.epage=e0154094&rft.pages=e0154094-e0154094&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0154094&rft_dat=%3Cgale_plos_%3EA453426675%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1783674536&rft_id=info:pmid/27105023&rft_galeid=A453426675&rft_doaj_id=oai_doaj_org_article_a2ea1a9274ca484aa642497dd616ba90&rfr_iscdi=true |