Differential transcriptional regulation of meis1 by Gfi1b and its co-factors LSD1 and CoREST
Gfi1b (growth factor independence 1b) is a zinc finger transcription factor essential for development of the erythroid and megakaryocytic lineages. To elucidate the mechanism underlying Gfi1b function, potential downstream transcriptional targets were identified by chromatin immunoprecipitation and...
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| creator | Chowdhury, Asif H Ramroop, Johnny R Upadhyay, Ghanshyam Sengupta, Ananya Andrzejczyk, Anna Saleque, Shireen |
| description | Gfi1b (growth factor independence 1b) is a zinc finger transcription factor essential for development of the erythroid and megakaryocytic lineages. To elucidate the mechanism underlying Gfi1b function, potential downstream transcriptional targets were identified by chromatin immunoprecipitation and expression profiling approaches. The combination of these approaches revealed the oncogene meis1, which encodes a homeobox protein, as a direct and prominent target of Gfi1b. Examination of the meis1 promoter sequence revealed multiple Gfi1/1b consensus binding motifs. Distinct regions of the promoter were occupied by Gfi1b and its cofactors LSD1 and CoREST/Rcor1, in erythroid cells but not in the closely related megakaryocyte lineage. Accordingly, Meis1 was significantly upregulated in LSD1 inhibited erythroid cells, but not in megakaryocytes. This lineage specific upregulation in Meis1 expression was accompanied by a parallel increase in di-methyl histone3 lysine4 levels in the Meis1 promoter in LSD1 inhibited, erythroid cells. Meis1 was also substantially upregulated in gfi1b-/- fetal liver cells along with its transcriptional partners Pbx1 and several Hox messages. Elevated Meis1 message levels persisted in gfi1b mutant fetal liver cells differentiated along the erythroid lineage, relative to wild type. However, cells differentiated along the megakaryocytic lineage, exhibited no difference in Meis1 levels between controls and mutants. Transfection experiments further demonstrated specific repression of meis1 promoter driven reporters by wild type Gfi1b but neither by a SNAG domain mutant nor by a DNA binding deficient one, thus confirming direct functional regulation of this promoter by the Gfi1b transcriptional complex. Overall, our results demonstrate direct yet differential regulation of meis1 transcription by Gfi1b in distinct hematopoietic lineages thus revealing it to be a common, albeit lineage specific, target of both Gfi1b and its paralog Gfi1. |
| doi_str_mv | 10.1371/journal.pone.0053666 |
| format | Article |
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To elucidate the mechanism underlying Gfi1b function, potential downstream transcriptional targets were identified by chromatin immunoprecipitation and expression profiling approaches. The combination of these approaches revealed the oncogene meis1, which encodes a homeobox protein, as a direct and prominent target of Gfi1b. Examination of the meis1 promoter sequence revealed multiple Gfi1/1b consensus binding motifs. Distinct regions of the promoter were occupied by Gfi1b and its cofactors LSD1 and CoREST/Rcor1, in erythroid cells but not in the closely related megakaryocyte lineage. Accordingly, Meis1 was significantly upregulated in LSD1 inhibited erythroid cells, but not in megakaryocytes. This lineage specific upregulation in Meis1 expression was accompanied by a parallel increase in di-methyl histone3 lysine4 levels in the Meis1 promoter in LSD1 inhibited, erythroid cells. Meis1 was also substantially upregulated in gfi1b-/- fetal liver cells along with its transcriptional partners Pbx1 and several Hox messages. Elevated Meis1 message levels persisted in gfi1b mutant fetal liver cells differentiated along the erythroid lineage, relative to wild type. However, cells differentiated along the megakaryocytic lineage, exhibited no difference in Meis1 levels between controls and mutants. Transfection experiments further demonstrated specific repression of meis1 promoter driven reporters by wild type Gfi1b but neither by a SNAG domain mutant nor by a DNA binding deficient one, thus confirming direct functional regulation of this promoter by the Gfi1b transcriptional complex. Overall, our results demonstrate direct yet differential regulation of meis1 transcription by Gfi1b in distinct hematopoietic lineages thus revealing it to be a common, albeit lineage specific, target of both Gfi1b and its paralog Gfi1.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0053666</identifier><identifier>PMID: 23308270</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Amino acids ; Animals ; Base Sequence ; Binding ; Binding Sites ; Biology ; Cell Differentiation ; Cell Line, Tumor ; Chromatin ; Cofactors ; Conserved sequence ; Deoxyribonucleic acid ; DNA ; DNA binding proteins ; Drosophila ; Erythroid cells ; Erythroid Cells - cytology ; Erythroid Cells - metabolism ; Fetus ; Fetuses ; Gene Expression Regulation ; Gene regulation ; Genes ; Hepatocytes ; Histone Demethylases ; Homeobox ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Humans ; Immunoprecipitation ; Insects ; Leukemia ; Liver ; Megakaryocytes ; Megakaryocytes - cytology ; Megakaryocytes - metabolism ; Mice ; Molecular Sequence Data ; Mutants ; Myeloid Ecotropic Viral Integration Site 1 Protein ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Oxidoreductases, N-Demethylating - genetics ; Oxidoreductases, N-Demethylating - metabolism ; Promoter Regions, Genetic ; Protein Binding ; Protein Structure, Tertiary ; Proteins ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Rodents ; Signal Transduction ; Target recognition ; Transcription (Genetics) ; Transcription, Genetic ; Transfection ; Zinc ; Zinc finger proteins</subject><ispartof>PloS one, 2013-01, Vol.8 (1), p.e53666-e53666</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Chowdhury et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://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>2013 Chowdhury et al 2013 Chowdhury et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-7f6bb0baacd9fdf7285e7a99d9c3e9f65dc32e8ccde0a41f512ef07e5b3cf5f33</citedby><cites>FETCH-LOGICAL-c758t-7f6bb0baacd9fdf7285e7a99d9c3e9f65dc32e8ccde0a41f512ef07e5b3cf5f33</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/PMC3538684/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3538684/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23308270$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Taneja, Reshma</contributor><creatorcontrib>Chowdhury, Asif H</creatorcontrib><creatorcontrib>Ramroop, Johnny R</creatorcontrib><creatorcontrib>Upadhyay, Ghanshyam</creatorcontrib><creatorcontrib>Sengupta, Ananya</creatorcontrib><creatorcontrib>Andrzejczyk, Anna</creatorcontrib><creatorcontrib>Saleque, Shireen</creatorcontrib><title>Differential transcriptional regulation of meis1 by Gfi1b and its co-factors LSD1 and CoREST</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Gfi1b (growth factor independence 1b) is a zinc finger transcription factor essential for development of the erythroid and megakaryocytic lineages. To elucidate the mechanism underlying Gfi1b function, potential downstream transcriptional targets were identified by chromatin immunoprecipitation and expression profiling approaches. The combination of these approaches revealed the oncogene meis1, which encodes a homeobox protein, as a direct and prominent target of Gfi1b. Examination of the meis1 promoter sequence revealed multiple Gfi1/1b consensus binding motifs. Distinct regions of the promoter were occupied by Gfi1b and its cofactors LSD1 and CoREST/Rcor1, in erythroid cells but not in the closely related megakaryocyte lineage. Accordingly, Meis1 was significantly upregulated in LSD1 inhibited erythroid cells, but not in megakaryocytes. This lineage specific upregulation in Meis1 expression was accompanied by a parallel increase in di-methyl histone3 lysine4 levels in the Meis1 promoter in LSD1 inhibited, erythroid cells. Meis1 was also substantially upregulated in gfi1b-/- fetal liver cells along with its transcriptional partners Pbx1 and several Hox messages. Elevated Meis1 message levels persisted in gfi1b mutant fetal liver cells differentiated along the erythroid lineage, relative to wild type. However, cells differentiated along the megakaryocytic lineage, exhibited no difference in Meis1 levels between controls and mutants. Transfection experiments further demonstrated specific repression of meis1 promoter driven reporters by wild type Gfi1b but neither by a SNAG domain mutant nor by a DNA binding deficient one, thus confirming direct functional regulation of this promoter by the Gfi1b transcriptional complex. Overall, our results demonstrate direct yet differential regulation of meis1 transcription by Gfi1b in distinct hematopoietic lineages thus revealing it to be a common, albeit lineage specific, target of both Gfi1b and its paralog Gfi1.</description><subject>Amino acids</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Binding</subject><subject>Binding Sites</subject><subject>Biology</subject><subject>Cell Differentiation</subject><subject>Cell Line, Tumor</subject><subject>Chromatin</subject><subject>Cofactors</subject><subject>Conserved sequence</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA binding proteins</subject><subject>Drosophila</subject><subject>Erythroid cells</subject><subject>Erythroid Cells - cytology</subject><subject>Erythroid Cells - metabolism</subject><subject>Fetus</subject><subject>Fetuses</subject><subject>Gene Expression Regulation</subject><subject>Gene regulation</subject><subject>Genes</subject><subject>Hepatocytes</subject><subject>Histone Demethylases</subject><subject>Homeobox</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Insects</subject><subject>Leukemia</subject><subject>Liver</subject><subject>Megakaryocytes</subject><subject>Megakaryocytes - cytology</subject><subject>Megakaryocytes - metabolism</subject><subject>Mice</subject><subject>Molecular Sequence Data</subject><subject>Mutants</subject><subject>Myeloid Ecotropic Viral Integration Site 1 Protein</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Oxidoreductases, N-Demethylating - genetics</subject><subject>Oxidoreductases, N-Demethylating - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Binding</subject><subject>Protein Structure, Tertiary</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Target recognition</subject><subject>Transcription (Genetics)</subject><subject>Transcription, Genetic</subject><subject>Transfection</subject><subject>Zinc</subject><subject>Zinc finger proteins</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</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>eNqNk1Fv0zAQxyMEYqPwDRBEQkLw0GLHdhK_IE3dGJUqTVoHT0iW45xbV2nc2Q5i3x5nzaYG7QHlIfH5d3_n_r5LkrcYzTAp8Jet7Vwrm9netjBDiJE8z58lp5iTbJpniDw_-j5JXnm_7aEyz18mJxkhqMwKdJr8Ojdag4M2GNmkwcnWK2f2wdionTpYd43sF6nV6Q6Mx2l1l15qg6tUtnVqgk-VnWqpgnU-Xa7O8X18bq8vVjevkxdaNh7eDO9J8uPbxc38-3R5dbmYny2nqmBlmBY6rypUSalqrmtdZCWDQnJec0WA65zVimRQKlUDkhRrhjPQqABWEaWZJmSSvD_o7hvrxWCMFzgreVlQRlAkFgeitnIr9s7spLsTVhpxH7BuLaQLRjUgKNBMMUx0xXMqCStrhRgnFENV8hiLWl-H07pqB7WK3jnZjETHO63ZiLX9LUhvf0mjwKdBwNnbDnwQO-MVNI1swXb9fxeEEk54j374B326uoFay1iAabWN56peVJzRoqQI41jQJJk9QcWnhp1RsYu0ifFRwudRQmQC_Alr2XkvFqvr_2evfo7Zj0fsBmQTNt42Xd9nfgzSA6ic9d6BfjQZI9EPwYMboh8CMQxBTHt3fEGPSQ9dT_4CgtYBHQ</recordid><startdate>20130107</startdate><enddate>20130107</enddate><creator>Chowdhury, Asif H</creator><creator>Ramroop, Johnny R</creator><creator>Upadhyay, Ghanshyam</creator><creator>Sengupta, Ananya</creator><creator>Andrzejczyk, Anna</creator><creator>Saleque, Shireen</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>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>20130107</creationdate><title>Differential transcriptional regulation of meis1 by Gfi1b and its co-factors LSD1 and CoREST</title><author>Chowdhury, Asif H ; Ramroop, Johnny R ; Upadhyay, Ghanshyam ; Sengupta, Ananya ; Andrzejczyk, Anna ; Saleque, Shireen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-7f6bb0baacd9fdf7285e7a99d9c3e9f65dc32e8ccde0a41f512ef07e5b3cf5f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Amino acids</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Binding</topic><topic>Binding Sites</topic><topic>Biology</topic><topic>Cell Differentiation</topic><topic>Cell Line, Tumor</topic><topic>Chromatin</topic><topic>Cofactors</topic><topic>Conserved sequence</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA binding proteins</topic><topic>Drosophila</topic><topic>Erythroid cells</topic><topic>Erythroid 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>Chowdhury, Asif H</au><au>Ramroop, Johnny R</au><au>Upadhyay, Ghanshyam</au><au>Sengupta, Ananya</au><au>Andrzejczyk, Anna</au><au>Saleque, Shireen</au><au>Taneja, Reshma</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential transcriptional regulation of meis1 by Gfi1b and its co-factors LSD1 and CoREST</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-01-07</date><risdate>2013</risdate><volume>8</volume><issue>1</issue><spage>e53666</spage><epage>e53666</epage><pages>e53666-e53666</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Gfi1b (growth factor independence 1b) is a zinc finger transcription factor essential for development of the erythroid and megakaryocytic lineages. To elucidate the mechanism underlying Gfi1b function, potential downstream transcriptional targets were identified by chromatin immunoprecipitation and expression profiling approaches. The combination of these approaches revealed the oncogene meis1, which encodes a homeobox protein, as a direct and prominent target of Gfi1b. Examination of the meis1 promoter sequence revealed multiple Gfi1/1b consensus binding motifs. Distinct regions of the promoter were occupied by Gfi1b and its cofactors LSD1 and CoREST/Rcor1, in erythroid cells but not in the closely related megakaryocyte lineage. Accordingly, Meis1 was significantly upregulated in LSD1 inhibited erythroid cells, but not in megakaryocytes. This lineage specific upregulation in Meis1 expression was accompanied by a parallel increase in di-methyl histone3 lysine4 levels in the Meis1 promoter in LSD1 inhibited, erythroid cells. Meis1 was also substantially upregulated in gfi1b-/- fetal liver cells along with its transcriptional partners Pbx1 and several Hox messages. Elevated Meis1 message levels persisted in gfi1b mutant fetal liver cells differentiated along the erythroid lineage, relative to wild type. However, cells differentiated along the megakaryocytic lineage, exhibited no difference in Meis1 levels between controls and mutants. Transfection experiments further demonstrated specific repression of meis1 promoter driven reporters by wild type Gfi1b but neither by a SNAG domain mutant nor by a DNA binding deficient one, thus confirming direct functional regulation of this promoter by the Gfi1b transcriptional complex. Overall, our results demonstrate direct yet differential regulation of meis1 transcription by Gfi1b in distinct hematopoietic lineages thus revealing it to be a common, albeit lineage specific, target of both Gfi1b and its paralog Gfi1.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23308270</pmid><doi>10.1371/journal.pone.0053666</doi><tpages>e53666</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-01, Vol.8 (1), p.e53666-e53666 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1289874530 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Amino acids Animals Base Sequence Binding Binding Sites Biology Cell Differentiation Cell Line, Tumor Chromatin Cofactors Conserved sequence Deoxyribonucleic acid DNA DNA binding proteins Drosophila Erythroid cells Erythroid Cells - cytology Erythroid Cells - metabolism Fetus Fetuses Gene Expression Regulation Gene regulation Genes Hepatocytes Histone Demethylases Homeobox Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Humans Immunoprecipitation Insects Leukemia Liver Megakaryocytes Megakaryocytes - cytology Megakaryocytes - metabolism Mice Molecular Sequence Data Mutants Myeloid Ecotropic Viral Integration Site 1 Protein Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Oxidoreductases, N-Demethylating - genetics Oxidoreductases, N-Demethylating - metabolism Promoter Regions, Genetic Protein Binding Protein Structure, Tertiary Proteins Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Repressor Proteins - genetics Repressor Proteins - metabolism Rodents Signal Transduction Target recognition Transcription (Genetics) Transcription, Genetic Transfection Zinc Zinc finger proteins |
| title | Differential transcriptional regulation of meis1 by Gfi1b and its co-factors LSD1 and CoREST |
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