The histone methyltransferase Setd8 alters the chromatin landscape and regulates the expression of key transcription factors during erythroid differentiation
Background SETD8 is the sole methyltransferase capable of mono-methylating histone H4, lysine 20. SETD8 and H4K20me1 play a role in a number of essential biologic processes, including cell cycle progression, establishment of higher order chromatin structure, and transcriptional regulation. SETD8 is...
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| description | Background SETD8 is the sole methyltransferase capable of mono-methylating histone H4, lysine 20. SETD8 and H4K20me1 play a role in a number of essential biologic processes, including cell cycle progression, establishment of higher order chromatin structure, and transcriptional regulation. SETD8 is highly expressed in erythroid cells and erythroid deletion of Setd8 is embryonic lethal by embryonic day 11.5 (E11.5) due to profound anemia, suggesting that it has an erythroid-specific function. The function of SETD8 in the hemopoietic system is poorly understood. The goal of our study was to gain insights into the function of SETD8 during erythroid differentiation. Results We performed ATAC-seq (assay for transposase-accessible chromatin) on sorted populations of E10.5 Setd8 mutant and control erythroblasts. Accessibility profiles were integrated with expression changes and a mark of heterochromatin (H3K27me3) performed in wild-type E10.5 erythroblasts to further understand the role of SETD8 in erythropoiesis. Data integration identified regions of greater chromatin accessibility in Setd8 mutant cells that co-located with H3K27me3 in wild-type E10.5 erythroblasts suggesting that these regions, and their associated genes, are repressed during normal erythropoiesis. The majority of these more accessible regions were located in promoters and they frequently co-located with the NFY complex. Pathway analysis of genes identified through data integration revealed stemness-related pathways. Among those genes were multiple transcriptional regulators active in multipotent progenitors, but repressed during erythroid differentiation including Hhex, Hlx, and Gata2. Consistent with a role for SETD8 in erythroid specification, SETD8 expression is up-regulated upon erythroid commitment, and Setd8 disruption impairs erythroid colony forming ability. Conclusion Taken together, our results suggest that SETD8 is an important regulator of the chromatin landscape during erythroid differentiation, particularly at promoters. Our results also identify a novel role for Setd8 in the establishment of appropriate patterns of lineage-restricted gene expression during erythroid differentiation. |
| doi_str_mv | 10.1186/s13072-020-00337-9 |
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SETD8 and H4K20me1 play a role in a number of essential biologic processes, including cell cycle progression, establishment of higher order chromatin structure, and transcriptional regulation. SETD8 is highly expressed in erythroid cells and erythroid deletion of Setd8 is embryonic lethal by embryonic day 11.5 (E11.5) due to profound anemia, suggesting that it has an erythroid-specific function. The function of SETD8 in the hemopoietic system is poorly understood. The goal of our study was to gain insights into the function of SETD8 during erythroid differentiation. Results We performed ATAC-seq (assay for transposase-accessible chromatin) on sorted populations of E10.5 Setd8 mutant and control erythroblasts. Accessibility profiles were integrated with expression changes and a mark of heterochromatin (H3K27me3) performed in wild-type E10.5 erythroblasts to further understand the role of SETD8 in erythropoiesis. Data integration identified regions of greater chromatin accessibility in Setd8 mutant cells that co-located with H3K27me3 in wild-type E10.5 erythroblasts suggesting that these regions, and their associated genes, are repressed during normal erythropoiesis. The majority of these more accessible regions were located in promoters and they frequently co-located with the NFY complex. Pathway analysis of genes identified through data integration revealed stemness-related pathways. Among those genes were multiple transcriptional regulators active in multipotent progenitors, but repressed during erythroid differentiation including Hhex, Hlx, and Gata2. Consistent with a role for SETD8 in erythroid specification, SETD8 expression is up-regulated upon erythroid commitment, and Setd8 disruption impairs erythroid colony forming ability. Conclusion Taken together, our results suggest that SETD8 is an important regulator of the chromatin landscape during erythroid differentiation, particularly at promoters. Our results also identify a novel role for Setd8 in the establishment of appropriate patterns of lineage-restricted gene expression during erythroid differentiation.</description><identifier>ISSN: 1756-8935</identifier><identifier>EISSN: 1756-8935</identifier><identifier>DOI: 10.1186/s13072-020-00337-9</identifier><identifier>PMID: 32178723</identifier><language>eng</language><publisher>LONDON: Springer Nature</publisher><subject>Analysis ; Anemia ; Animals ; Cell cycle ; Cell Line ; Cells, Cultured ; Chromatin ; Chromatin Assembly and Disassembly ; Deoxyribonucleic acid ; Differentiation ; DNA ; DNA binding proteins ; DNA damage ; DNA methylation ; Embryos ; Epigenetics ; Erythroblasts - cytology ; Erythroblasts - metabolism ; Erythroid ; Erythropoiesis ; Gene expression ; Genes ; Genetic research ; Genetics & Heredity ; H4K20me1 ; Histone methyltransferase ; Histone-Lysine N-Methyltransferase - genetics ; Histone-Lysine N-Methyltransferase - metabolism ; Histones ; Humans ; Life Sciences & Biomedicine ; Lysine ; Methyltransferases ; Mice ; Mutants ; Novels ; Science & Technology ; Setd8 ; Transcription factors ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transferases</subject><ispartof>Epigenetics & chromatin, 2020-03, Vol.13 (1), p.16-16, Article 16</ispartof><rights>COPYRIGHT 2020 BioMed Central Ltd.</rights><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>17</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000521265800001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c597t-6e650c9c26576fb820ea8a6f18b28829bfba8af22b4a0964232f4cfb23fdbfdc3</citedby><cites>FETCH-LOGICAL-c597t-6e650c9c26576fb820ea8a6f18b28829bfba8af22b4a0964232f4cfb23fdbfdc3</cites><orcidid>0000-0002-2987-0400 ; 0000-0002-2923-4105</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7075014/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7075014/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,2106,2118,27933,27934,28257,53800,53802</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32178723$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Myers, Jacquelyn A.</creatorcontrib><creatorcontrib>Couch, Tyler</creatorcontrib><creatorcontrib>Murphy, Zachary</creatorcontrib><creatorcontrib>Malik, Jeffrey</creatorcontrib><creatorcontrib>Getman, Michael</creatorcontrib><creatorcontrib>Steiner, Laurie A.</creatorcontrib><title>The histone methyltransferase Setd8 alters the chromatin landscape and regulates the expression of key transcription factors during erythroid differentiation</title><title>Epigenetics & chromatin</title><addtitle>EPIGENET CHROMATIN</addtitle><addtitle>Epigenetics Chromatin</addtitle><description>Background SETD8 is the sole methyltransferase capable of mono-methylating histone H4, lysine 20. SETD8 and H4K20me1 play a role in a number of essential biologic processes, including cell cycle progression, establishment of higher order chromatin structure, and transcriptional regulation. SETD8 is highly expressed in erythroid cells and erythroid deletion of Setd8 is embryonic lethal by embryonic day 11.5 (E11.5) due to profound anemia, suggesting that it has an erythroid-specific function. The function of SETD8 in the hemopoietic system is poorly understood. The goal of our study was to gain insights into the function of SETD8 during erythroid differentiation. Results We performed ATAC-seq (assay for transposase-accessible chromatin) on sorted populations of E10.5 Setd8 mutant and control erythroblasts. Accessibility profiles were integrated with expression changes and a mark of heterochromatin (H3K27me3) performed in wild-type E10.5 erythroblasts to further understand the role of SETD8 in erythropoiesis. Data integration identified regions of greater chromatin accessibility in Setd8 mutant cells that co-located with H3K27me3 in wild-type E10.5 erythroblasts suggesting that these regions, and their associated genes, are repressed during normal erythropoiesis. The majority of these more accessible regions were located in promoters and they frequently co-located with the NFY complex. Pathway analysis of genes identified through data integration revealed stemness-related pathways. Among those genes were multiple transcriptional regulators active in multipotent progenitors, but repressed during erythroid differentiation including Hhex, Hlx, and Gata2. Consistent with a role for SETD8 in erythroid specification, SETD8 expression is up-regulated upon erythroid commitment, and Setd8 disruption impairs erythroid colony forming ability. Conclusion Taken together, our results suggest that SETD8 is an important regulator of the chromatin landscape during erythroid differentiation, particularly at promoters. Our results also identify a novel role for Setd8 in the establishment of appropriate patterns of lineage-restricted gene expression during erythroid differentiation.</description><subject>Analysis</subject><subject>Anemia</subject><subject>Animals</subject><subject>Cell cycle</subject><subject>Cell Line</subject><subject>Cells, Cultured</subject><subject>Chromatin</subject><subject>Chromatin Assembly and Disassembly</subject><subject>Deoxyribonucleic acid</subject><subject>Differentiation</subject><subject>DNA</subject><subject>DNA binding proteins</subject><subject>DNA damage</subject><subject>DNA methylation</subject><subject>Embryos</subject><subject>Epigenetics</subject><subject>Erythroblasts - cytology</subject><subject>Erythroblasts - metabolism</subject><subject>Erythroid</subject><subject>Erythropoiesis</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic research</subject><subject>Genetics & Heredity</subject><subject>H4K20me1</subject><subject>Histone methyltransferase</subject><subject>Histone-Lysine N-Methyltransferase - genetics</subject><subject>Histone-Lysine N-Methyltransferase - metabolism</subject><subject>Histones</subject><subject>Humans</subject><subject>Life Sciences & Biomedicine</subject><subject>Lysine</subject><subject>Methyltransferases</subject><subject>Mice</subject><subject>Mutants</subject><subject>Novels</subject><subject>Science & Technology</subject><subject>Setd8</subject><subject>Transcription factors</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transferases</subject><issn>1756-8935</issn><issn>1756-8935</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><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>eNqNkk1v1DAQhiMEolD4AxyQJS4glOKPJHYuSNWKj0qVkGg5W44z3nXJxovtQPfH8F-Z7JbSRRxQDplMnnksj96ieMboCWOqeZOYoJKXlNOSUiFk2d4rHjFZN6VqRX3_Tn1UPE7pitKGq4o-LI4EZ1JJLh4VPy9XQFY-5TACWUNebYcczZgcRJOAXEDuFTFDhphIRtSuYlib7EcymLFP1myAYEEiLKfBZNhTcL2JkJIPIwmOfIUt2Ult9Js8N52xOaCxn6IflwTiNqPX96T3Dk-GMXszg0-KB84MCZ7evI-LL-_fXS4-luefPpwtTs9LW7cylw00NbWt5U0tG9cpTsEo0zimOq4UbzvX4bfjvKsMbZuKC-4q6zouXN-53orj4mzv7YO50pvo1yZudTBe7xohLrWJ2dsBNGdQO8mlaZu6qh1VwETj6FxUVCqKrrd712bq1tBbvEw0w4H08M_oV3oZvmtJZU1ZhYKXN4IYvk2Qsl77ZGHAhUOYkuZCyrbFS0hEX_yFXoUpjriqmVKqFrRVf6ilwQv40QU8185SfdowJauaqtl18g8Knx7W3mI8nMf-wcCrgwFkMlznpZlS0mcXnw9ZvmdtDClFcLf7YFTPYdb7MGsMs96FWbc49PzuJm9HfqcXgdd74Ad0wSXrYbRwi1FKa84wEworypBW_08vfN4lcBGmMYtfvjAS4g</recordid><startdate>20200316</startdate><enddate>20200316</enddate><creator>Myers, Jacquelyn A.</creator><creator>Couch, Tyler</creator><creator>Murphy, Zachary</creator><creator>Malik, Jeffrey</creator><creator>Getman, Michael</creator><creator>Steiner, Laurie A.</creator><general>Springer Nature</general><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</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>ISR</scope><scope>3V.</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-2987-0400</orcidid><orcidid>https://orcid.org/0000-0002-2923-4105</orcidid></search><sort><creationdate>20200316</creationdate><title>The histone methyltransferase Setd8 alters the chromatin landscape and regulates the expression of key transcription factors during erythroid differentiation</title><author>Myers, Jacquelyn A. ; Couch, Tyler ; Murphy, Zachary ; Malik, Jeffrey ; Getman, Michael ; Steiner, Laurie A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c597t-6e650c9c26576fb820ea8a6f18b28829bfba8af22b4a0964232f4cfb23fdbfdc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Analysis</topic><topic>Anemia</topic><topic>Animals</topic><topic>Cell cycle</topic><topic>Cell Line</topic><topic>Cells, Cultured</topic><topic>Chromatin</topic><topic>Chromatin Assembly and Disassembly</topic><topic>Deoxyribonucleic acid</topic><topic>Differentiation</topic><topic>DNA</topic><topic>DNA binding proteins</topic><topic>DNA damage</topic><topic>DNA methylation</topic><topic>Embryos</topic><topic>Epigenetics</topic><topic>Erythroblasts - cytology</topic><topic>Erythroblasts - metabolism</topic><topic>Erythroid</topic><topic>Erythropoiesis</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genetic research</topic><topic>Genetics & Heredity</topic><topic>H4K20me1</topic><topic>Histone methyltransferase</topic><topic>Histone-Lysine N-Methyltransferase - genetics</topic><topic>Histone-Lysine N-Methyltransferase - metabolism</topic><topic>Histones</topic><topic>Humans</topic><topic>Life Sciences & Biomedicine</topic><topic>Lysine</topic><topic>Methyltransferases</topic><topic>Mice</topic><topic>Mutants</topic><topic>Novels</topic><topic>Science & Technology</topic><topic>Setd8</topic><topic>Transcription factors</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Transferases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Myers, Jacquelyn A.</creatorcontrib><creatorcontrib>Couch, Tyler</creatorcontrib><creatorcontrib>Murphy, Zachary</creatorcontrib><creatorcontrib>Malik, Jeffrey</creatorcontrib><creatorcontrib>Getman, Michael</creatorcontrib><creatorcontrib>Steiner, Laurie A.</creatorcontrib><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Epigenetics & chromatin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Myers, Jacquelyn A.</au><au>Couch, Tyler</au><au>Murphy, Zachary</au><au>Malik, Jeffrey</au><au>Getman, Michael</au><au>Steiner, Laurie A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The histone methyltransferase Setd8 alters the chromatin landscape and regulates the expression of key transcription factors during erythroid differentiation</atitle><jtitle>Epigenetics & chromatin</jtitle><stitle>EPIGENET CHROMATIN</stitle><addtitle>Epigenetics Chromatin</addtitle><date>2020-03-16</date><risdate>2020</risdate><volume>13</volume><issue>1</issue><spage>16</spage><epage>16</epage><pages>16-16</pages><artnum>16</artnum><issn>1756-8935</issn><eissn>1756-8935</eissn><abstract>Background SETD8 is the sole methyltransferase capable of mono-methylating histone H4, lysine 20. SETD8 and H4K20me1 play a role in a number of essential biologic processes, including cell cycle progression, establishment of higher order chromatin structure, and transcriptional regulation. SETD8 is highly expressed in erythroid cells and erythroid deletion of Setd8 is embryonic lethal by embryonic day 11.5 (E11.5) due to profound anemia, suggesting that it has an erythroid-specific function. The function of SETD8 in the hemopoietic system is poorly understood. The goal of our study was to gain insights into the function of SETD8 during erythroid differentiation. Results We performed ATAC-seq (assay for transposase-accessible chromatin) on sorted populations of E10.5 Setd8 mutant and control erythroblasts. Accessibility profiles were integrated with expression changes and a mark of heterochromatin (H3K27me3) performed in wild-type E10.5 erythroblasts to further understand the role of SETD8 in erythropoiesis. Data integration identified regions of greater chromatin accessibility in Setd8 mutant cells that co-located with H3K27me3 in wild-type E10.5 erythroblasts suggesting that these regions, and their associated genes, are repressed during normal erythropoiesis. The majority of these more accessible regions were located in promoters and they frequently co-located with the NFY complex. Pathway analysis of genes identified through data integration revealed stemness-related pathways. Among those genes were multiple transcriptional regulators active in multipotent progenitors, but repressed during erythroid differentiation including Hhex, Hlx, and Gata2. Consistent with a role for SETD8 in erythroid specification, SETD8 expression is up-regulated upon erythroid commitment, and Setd8 disruption impairs erythroid colony forming ability. Conclusion Taken together, our results suggest that SETD8 is an important regulator of the chromatin landscape during erythroid differentiation, particularly at promoters. Our results also identify a novel role for Setd8 in the establishment of appropriate patterns of lineage-restricted gene expression during erythroid differentiation.</abstract><cop>LONDON</cop><pub>Springer Nature</pub><pmid>32178723</pmid><doi>10.1186/s13072-020-00337-9</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-2987-0400</orcidid><orcidid>https://orcid.org/0000-0002-2923-4105</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Anemia Animals Cell cycle Cell Line Cells, Cultured Chromatin Chromatin Assembly and Disassembly Deoxyribonucleic acid Differentiation DNA DNA binding proteins DNA damage DNA methylation Embryos Epigenetics Erythroblasts - cytology Erythroblasts - metabolism Erythroid Erythropoiesis Gene expression Genes Genetic research Genetics & Heredity H4K20me1 Histone methyltransferase Histone-Lysine N-Methyltransferase - genetics Histone-Lysine N-Methyltransferase - metabolism Histones Humans Life Sciences & Biomedicine Lysine Methyltransferases Mice Mutants Novels Science & Technology Setd8 Transcription factors Transcription Factors - genetics Transcription Factors - metabolism Transferases |
| title | The histone methyltransferase Setd8 alters the chromatin landscape and regulates the expression of key transcription factors during erythroid differentiation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-11-29T20%3A43%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20histone%20methyltransferase%20Setd8%20alters%20the%20chromatin%20landscape%20and%20regulates%20the%20expression%20of%20key%20transcription%20factors%20during%20erythroid%20differentiation&rft.jtitle=Epigenetics%20&%20chromatin&rft.au=Myers,%20Jacquelyn%20A.&rft.date=2020-03-16&rft.volume=13&rft.issue=1&rft.spage=16&rft.epage=16&rft.pages=16-16&rft.artnum=16&rft.issn=1756-8935&rft.eissn=1756-8935&rft_id=info:doi/10.1186/s13072-020-00337-9&rft_dat=%3Cgale_proqu%3EA618745087%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2378853098&rft_id=info:pmid/32178723&rft_galeid=A618745087&rft_doaj_id=oai_doaj_org_article_21e5f727a96545f08e136f0f08e40780&rfr_iscdi=true |