HoxB domain induction silences DNA replication origins in the locus and specifies a single origin at its boundary
In multicellular organisms, changes in the DNA replication programme could act to integrate differentiation with cell division in various developmental and transcriptional contexts. Here, we have addressed the use of DNA replication origins during differentiation in the HoxB domain—a cluster of nine...
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description | In multicellular organisms, changes in the DNA replication programme could act to integrate differentiation with cell division in various developmental and transcriptional contexts. Here, we have addressed the use of DNA replication origins during differentiation in the HoxB domain—a cluster of nine genes developmentally regulated in a collinear manner. In undifferentiated mouse P19 cells, we detected several DNA replication origins in the 100 kb HoxB locus, indicating a relaxed origin use when the locus is transcriptionally silent. By contrast, in retinoic‐acid‐induced differentiated cells, when HoxB transcription is activated, a general silencing of DNA replication origins occurs in the locus except one located downstream of
Hoxb1
, at the 3′ boundary of the HoxB domain. Silencing of the replication origins is associated with histone hyperacetylation, whereas the active
Hoxb1
origin persists as a hypoacetylated island. These findings provide direct evidence for the differentiated use of origins in HoxB genes, and we suggest that this regulation might contribute to the regulated expression of HoxB genes during development. |
doi_str_mv | 10.1038/sj.embor.7400758 |
format | Article |
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Hoxb1
, at the 3′ boundary of the HoxB domain. Silencing of the replication origins is associated with histone hyperacetylation, whereas the active
Hoxb1
origin persists as a hypoacetylated island. These findings provide direct evidence for the differentiated use of origins in HoxB genes, and we suggest that this regulation might contribute to the regulated expression of HoxB genes during development.</description><identifier>ISSN: 1469-221X</identifier><identifier>EISSN: 1469-3178</identifier><identifier>EISSN: 1469-221X</identifier><identifier>DOI: 10.1038/sj.embor.7400758</identifier><identifier>PMID: 16845368</identifier><identifier>CODEN: ERMEAX</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Acetylation ; Animals ; Cell Differentiation - drug effects ; Cell Differentiation - genetics ; Cell Differentiation - physiology ; Cell Line, Tumor ; Chromatin Immunoprecipitation ; Deoxyribonucleic acid ; DNA ; DNA Replication - genetics ; Gene expression ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - genetics ; Gene loci ; Genetics ; Histones - genetics ; Histones - metabolism ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Human genetics ; Life Sciences ; Models, Genetic ; Origin Recognition Complex - genetics ; Origin Recognition Complex - metabolism ; Prenatal development ; Replication Origin - genetics ; Rodents ; Scientific Report ; Scientific Reports ; Transcription, Genetic - drug effects ; Transcription, Genetic - genetics ; Tretinoin - pharmacology</subject><ispartof>EMBO reports, 2006-08, Vol.7 (8), p.812-816</ispartof><rights>European Molecular Biology Organization 2006</rights><rights>Copyright © 2006 European Molecular Biology Organization</rights><rights>Copyright Nature Publishing Group Aug 2006</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>Copyright © 2006, European Molecular Biology Organization 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6828-1b0af93129821e861e1c90b33445243bcd792335b95120acf5e576d5a043377f3</citedby><cites>FETCH-LOGICAL-c6828-1b0af93129821e861e1c90b33445243bcd792335b95120acf5e576d5a043377f3</cites><orcidid>0000-0003-3124-7586</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/PMC1525151/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1525151/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16845368$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00113404$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Grégoire, Damien</creatorcontrib><creatorcontrib>Brodolin, Konstantin</creatorcontrib><creatorcontrib>Méchali, Marcel</creatorcontrib><title>HoxB domain induction silences DNA replication origins in the locus and specifies a single origin at its boundary</title><title>EMBO reports</title><addtitle>EMBO Rep</addtitle><addtitle>EMBO Rep</addtitle><description>In multicellular organisms, changes in the DNA replication programme could act to integrate differentiation with cell division in various developmental and transcriptional contexts. Here, we have addressed the use of DNA replication origins during differentiation in the HoxB domain—a cluster of nine genes developmentally regulated in a collinear manner. In undifferentiated mouse P19 cells, we detected several DNA replication origins in the 100 kb HoxB locus, indicating a relaxed origin use when the locus is transcriptionally silent. By contrast, in retinoic‐acid‐induced differentiated cells, when HoxB transcription is activated, a general silencing of DNA replication origins occurs in the locus except one located downstream of
Hoxb1
, at the 3′ boundary of the HoxB domain. Silencing of the replication origins is associated with histone hyperacetylation, whereas the active
Hoxb1
origin persists as a hypoacetylated island. These findings provide direct evidence for the differentiated use of origins in HoxB genes, and we suggest that this regulation might contribute to the regulated expression of HoxB genes during development.</description><subject>Acetylation</subject><subject>Animals</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Differentiation - genetics</subject><subject>Cell Differentiation - physiology</subject><subject>Cell Line, Tumor</subject><subject>Chromatin Immunoprecipitation</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Replication - genetics</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - genetics</subject><subject>Gene loci</subject><subject>Genetics</subject><subject>Histones - genetics</subject><subject>Histones - metabolism</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Human genetics</subject><subject>Life Sciences</subject><subject>Models, Genetic</subject><subject>Origin Recognition Complex - genetics</subject><subject>Origin Recognition Complex - metabolism</subject><subject>Prenatal development</subject><subject>Replication Origin - genetics</subject><subject>Rodents</subject><subject>Scientific Report</subject><subject>Scientific Reports</subject><subject>Transcription, Genetic - drug effects</subject><subject>Transcription, Genetic - genetics</subject><subject>Tretinoin - pharmacology</subject><issn>1469-221X</issn><issn>1469-3178</issn><issn>1469-221X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFks1v0zAYxiMEYmNw54QsDkgcWuw4_rogdZ8FlSIhEIiL5ThO65LYnZ2M7b_HXaIVdmAnW_bved5Hr54se4ngFEHM38XN1LSlD1NWQMgIf5QdooKKCUaMPx7veY5-HGTPYtxACIlg_Gl2gCgvCKb8MLuc--tjUPlWWQesq3rdWe9AtI1x2kRwupyBYLaN1er2wwe7si4mFHRrAxqv-wiUq0DcGm1rmyQqqd2qMSMLVAdsF0Hpe1epcPM8e1KrJpoX43mUfTs_-3oynyw-X3w4mS0mmvKcT1AJVS0wygXPkeEUGaQFLDEuCpIXuNQVEznGpBQE5VDpmhjCaEUULDBmrMZH2fvBd9uXram0cV1QjdwG26YU0isr__1xdi1X_koikhNEUDJ4Oxis78nms4XcvUGIEC5gcbVj34zDgr_sTexka6M2TaOc8X2UlFMhKH0YRIyKXIgiga_vgRvfB5c2JnPI0wogowmCA6SDjzGY-i4ngnLXEBk38rYhcmxIkrz6ey17wViJBIgB-J06cPOgoTz7dPxlb44GbUwytzJhH_o_gSaDxsbOXN_NU-GXpAwzIr8vL-Q5_LmApx-FXOI_firp9w</recordid><startdate>200608</startdate><enddate>200608</enddate><creator>Grégoire, Damien</creator><creator>Brodolin, Konstantin</creator><creator>Méchali, Marcel</creator><general>John Wiley & Sons, Ltd</general><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><general>EMBO Press</general><scope>BSCLL</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>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3124-7586</orcidid></search><sort><creationdate>200608</creationdate><title>HoxB domain induction silences DNA replication origins in the locus and specifies a single origin at its boundary</title><author>Grégoire, Damien ; Brodolin, Konstantin ; Méchali, Marcel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6828-1b0af93129821e861e1c90b33445243bcd792335b95120acf5e576d5a043377f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Acetylation</topic><topic>Animals</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Differentiation - genetics</topic><topic>Cell Differentiation - physiology</topic><topic>Cell Line, Tumor</topic><topic>Chromatin Immunoprecipitation</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Replication - genetics</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Expression Regulation - genetics</topic><topic>Gene loci</topic><topic>Genetics</topic><topic>Histones - genetics</topic><topic>Histones - metabolism</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Human genetics</topic><topic>Life Sciences</topic><topic>Models, Genetic</topic><topic>Origin Recognition Complex - genetics</topic><topic>Origin Recognition Complex - metabolism</topic><topic>Prenatal development</topic><topic>Replication Origin - genetics</topic><topic>Rodents</topic><topic>Scientific Report</topic><topic>Scientific Reports</topic><topic>Transcription, Genetic - drug effects</topic><topic>Transcription, Genetic - genetics</topic><topic>Tretinoin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Grégoire, Damien</creatorcontrib><creatorcontrib>Brodolin, Konstantin</creatorcontrib><creatorcontrib>Méchali, Marcel</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</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>Environmental Sciences and Pollution Management</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>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</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>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>EMBO reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Grégoire, Damien</au><au>Brodolin, Konstantin</au><au>Méchali, Marcel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HoxB domain induction silences DNA replication origins in the locus and specifies a single origin at its boundary</atitle><jtitle>EMBO reports</jtitle><stitle>EMBO Rep</stitle><addtitle>EMBO Rep</addtitle><date>2006-08</date><risdate>2006</risdate><volume>7</volume><issue>8</issue><spage>812</spage><epage>816</epage><pages>812-816</pages><issn>1469-221X</issn><eissn>1469-3178</eissn><eissn>1469-221X</eissn><coden>ERMEAX</coden><abstract>In multicellular organisms, changes in the DNA replication programme could act to integrate differentiation with cell division in various developmental and transcriptional contexts. Here, we have addressed the use of DNA replication origins during differentiation in the HoxB domain—a cluster of nine genes developmentally regulated in a collinear manner. In undifferentiated mouse P19 cells, we detected several DNA replication origins in the 100 kb HoxB locus, indicating a relaxed origin use when the locus is transcriptionally silent. By contrast, in retinoic‐acid‐induced differentiated cells, when HoxB transcription is activated, a general silencing of DNA replication origins occurs in the locus except one located downstream of
Hoxb1
, at the 3′ boundary of the HoxB domain. Silencing of the replication origins is associated with histone hyperacetylation, whereas the active
Hoxb1
origin persists as a hypoacetylated island. These findings provide direct evidence for the differentiated use of origins in HoxB genes, and we suggest that this regulation might contribute to the regulated expression of HoxB genes during development.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>16845368</pmid><doi>10.1038/sj.embor.7400758</doi><tpages>5</tpages><orcidid>https://orcid.org/0000-0003-3124-7586</orcidid><oa>free_for_read</oa></addata></record> |
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source | Wiley Free Content; MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
subjects | Acetylation Animals Cell Differentiation - drug effects Cell Differentiation - genetics Cell Differentiation - physiology Cell Line, Tumor Chromatin Immunoprecipitation Deoxyribonucleic acid DNA DNA Replication - genetics Gene expression Gene Expression Regulation - drug effects Gene Expression Regulation - genetics Gene loci Genetics Histones - genetics Histones - metabolism Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Human genetics Life Sciences Models, Genetic Origin Recognition Complex - genetics Origin Recognition Complex - metabolism Prenatal development Replication Origin - genetics Rodents Scientific Report Scientific Reports Transcription, Genetic - drug effects Transcription, Genetic - genetics Tretinoin - pharmacology |
title | HoxB domain induction silences DNA replication origins in the locus and specifies a single origin at its boundary |
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