Spatiotemporal regulation of endothelin receptor-B by SOX10 in neural crest-derived enteric neuron precursors
Hirschsprung disease (HSCR) is a multigenic, congenital disorder that affects 1 in 5,000 newborns and is characterized by the absence of neural crest-derived enteric ganglia in the colon. One of the primary genes affected in HSCR encodes the G protein-coupled endothelin receptor-B (EDNRB). The expre...
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| Veröffentlicht in: | Nature genetics 2004-07, Vol.36 (7), p.732-737 |
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| creator | Shin, Myung K Zhu, Lei Lee, Hyung-Ok Jordan, ChaRandle S Cantrell, V Ashley Southard-Smith, E Michelle |
| description | Hirschsprung disease (HSCR) is a multigenic, congenital disorder that affects 1 in 5,000 newborns and is characterized by the absence of neural crest-derived enteric ganglia in the colon. One of the primary genes affected in HSCR encodes the G protein-coupled endothelin receptor-B (EDNRB). The expression of Ednrb is required at a defined time period during the migration of the precursors of the enteric nervous system (ENS) into the colon. In this study, we describe a conserved spatiotemporal ENS enhancer of Ednrb. This 1-kb enhancer is activated as the ENS precursors approach the colon, and partial deletion of this enhancer at the endogenous Ednrb locus results in pigmented mice that die postnatally from megacolon. We identified binding sites for SOX10, an SRY-related transcription factor associated with HSCR, in the Ednrb ENS enhancer, and mutational analyses of these sites suggested that SOX10 may have multiple roles in regulating Ednrb in the ENS. |
| doi_str_mv | 10.1038/ng1371 |
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One of the primary genes affected in HSCR encodes the G protein-coupled endothelin receptor-B (EDNRB). The expression of Ednrb is required at a defined time period during the migration of the precursors of the enteric nervous system (ENS) into the colon. In this study, we describe a conserved spatiotemporal ENS enhancer of Ednrb. This 1-kb enhancer is activated as the ENS precursors approach the colon, and partial deletion of this enhancer at the endogenous Ednrb locus results in pigmented mice that die postnatally from megacolon. We identified binding sites for SOX10, an SRY-related transcription factor associated with HSCR, in the Ednrb ENS enhancer, and mutational analyses of these sites suggested that SOX10 may have multiple roles in regulating Ednrb in the ENS.</description><identifier>ISSN: 1061-4036</identifier><identifier>EISSN: 1546-1718</identifier><identifier>DOI: 10.1038/ng1371</identifier><identifier>PMID: 15170213</identifier><identifier>CODEN: NGENEC</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Agriculture ; Animal Genetics and Genomics ; Animals ; Base Sequence ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell receptors ; Cell structures and functions ; Cloning ; Complications and side effects ; Diagnosis ; Enhancer Elements, Genetic ; Enteric Nervous System - physiology ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Gene Expression Regulation - physiology ; Gene Function ; Gene mutations ; Genetic aspects ; Genetics of eukaryotes. Biological and molecular evolution ; Health aspects ; High Mobility Group Proteins - physiology ; Hirschsprung's disease ; Human Genetics ; letter ; Mice ; Mice, Transgenic ; Miscellaneous ; Molecular and cellular biology ; Molecular Sequence Data ; Mutation ; Neoplasm Proteins - physiology ; Receptors, Endothelin - genetics ; Risk factors ; Sequence Homology, Nucleic Acid ; SOXE Transcription Factors ; Transcription Factors</subject><ispartof>Nature genetics, 2004-07, Vol.36 (7), p.732-737</ispartof><rights>Springer Nature America, Inc. 2004</rights><rights>2005 INIST-CNRS</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jul 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c649t-555fdc6ab5a534737d98e029f4f8d61a9570267df87e395c14c13051e14268a93</citedby><cites>FETCH-LOGICAL-c649t-555fdc6ab5a534737d98e029f4f8d61a9570267df87e395c14c13051e14268a93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2727,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15956544$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15170213$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shin, Myung K</creatorcontrib><creatorcontrib>Zhu, Lei</creatorcontrib><creatorcontrib>Lee, Hyung-Ok</creatorcontrib><creatorcontrib>Jordan, ChaRandle S</creatorcontrib><creatorcontrib>Cantrell, V Ashley</creatorcontrib><creatorcontrib>Southard-Smith, E Michelle</creatorcontrib><title>Spatiotemporal regulation of endothelin receptor-B by SOX10 in neural crest-derived enteric neuron precursors</title><title>Nature genetics</title><addtitle>Nat Genet</addtitle><addtitle>Nat Genet</addtitle><description>Hirschsprung disease (HSCR) is a multigenic, congenital disorder that affects 1 in 5,000 newborns and is characterized by the absence of neural crest-derived enteric ganglia in the colon. One of the primary genes affected in HSCR encodes the G protein-coupled endothelin receptor-B (EDNRB). The expression of Ednrb is required at a defined time period during the migration of the precursors of the enteric nervous system (ENS) into the colon. In this study, we describe a conserved spatiotemporal ENS enhancer of Ednrb. This 1-kb enhancer is activated as the ENS precursors approach the colon, and partial deletion of this enhancer at the endogenous Ednrb locus results in pigmented mice that die postnatally from megacolon. We identified binding sites for SOX10, an SRY-related transcription factor associated with HSCR, in the Ednrb ENS enhancer, and mutational analyses of these sites suggested that SOX10 may have multiple roles in regulating Ednrb in the ENS.</description><subject>Agriculture</subject><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cell receptors</subject><subject>Cell structures and functions</subject><subject>Cloning</subject><subject>Complications and side effects</subject><subject>Diagnosis</subject><subject>Enhancer Elements, Genetic</subject><subject>Enteric Nervous System - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - physiology</subject><subject>Gene Function</subject><subject>Gene mutations</subject><subject>Genetic aspects</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>Health aspects</subject><subject>High Mobility Group Proteins - physiology</subject><subject>Hirschsprung's disease</subject><subject>Human Genetics</subject><subject>letter</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Miscellaneous</subject><subject>Molecular and cellular biology</subject><subject>Molecular Sequence Data</subject><subject>Mutation</subject><subject>Neoplasm Proteins - physiology</subject><subject>Receptors, Endothelin - genetics</subject><subject>Risk factors</subject><subject>Sequence Homology, Nucleic Acid</subject><subject>SOXE Transcription Factors</subject><subject>Transcription Factors</subject><issn>1061-4036</issn><issn>1546-1718</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkt9v1DAMxysEYmPAX4BQBQLEQ0fc_Gj7OCYGkyadxAHircql7tGpTUqSIvbf41srxgESJA-x7M_XsS0nyUNgx8B4-cpugRdwKzkEKVQGBZS3yWYKMsG4OkjuhXDJGAjByrvJAUgoWA78MBnWo46diziMzus-9bid-p3Hpq5N0TYufsG-sxQwOEbns9fp5ipdrz4DS8ltcdrJjMcQswZ99w0bkkWyzHWQEo2knXxwPtxP7rS6D_hgeY-Sj2dvPpy-yy5Wb89PTy4yo0QVMyll2xilN1JLLgpeNFWJLK9a0ZaNAl1Jql4VTVsWyCtpQBjgTAKCyFWpK36UPJ_zjt59nai0euiCwb7XFt0UakWnKIp_g1AyyGm-BD75Dbx0k7fURJ3nuRKlVIqgpzO01T3WnW1d9NrsMtYnUHIBkPOcqOO_UHQbHDrjLLYd-fcEL_cExET8Hrd6CqE-X7__f3b1aZ9dmjfeheCxrUffDdpf1cDq3VbV81YR-HhpftoM2NxgyxoR8GwBdDC6b722pgu_cJVUUgjiXsxcoJDdor-Z4h9fPppJq-Pk8WeqJfwDmpLmbw</recordid><startdate>20040701</startdate><enddate>20040701</enddate><creator>Shin, Myung K</creator><creator>Zhu, Lei</creator><creator>Lee, Hyung-Ok</creator><creator>Jordan, ChaRandle S</creator><creator>Cantrell, V Ashley</creator><creator>Southard-Smith, E Michelle</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>IQODW</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</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>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></search><sort><creationdate>20040701</creationdate><title>Spatiotemporal regulation of endothelin receptor-B by SOX10 in neural crest-derived enteric neuron precursors</title><author>Shin, Myung K ; Zhu, Lei ; Lee, Hyung-Ok ; Jordan, ChaRandle S ; Cantrell, V Ashley ; Southard-Smith, E Michelle</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c649t-555fdc6ab5a534737d98e029f4f8d61a9570267df87e395c14c13051e14268a93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Agriculture</topic><topic>Animal Genetics and Genomics</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cell receptors</topic><topic>Cell structures and functions</topic><topic>Cloning</topic><topic>Complications and side effects</topic><topic>Diagnosis</topic><topic>Enhancer Elements, Genetic</topic><topic>Enteric Nervous System - physiology</topic><topic>Fundamental and applied biological sciences. 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Academic</collection><jtitle>Nature genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shin, Myung K</au><au>Zhu, Lei</au><au>Lee, Hyung-Ok</au><au>Jordan, ChaRandle S</au><au>Cantrell, V Ashley</au><au>Southard-Smith, E Michelle</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Spatiotemporal regulation of endothelin receptor-B by SOX10 in neural crest-derived enteric neuron precursors</atitle><jtitle>Nature genetics</jtitle><stitle>Nat Genet</stitle><addtitle>Nat Genet</addtitle><date>2004-07-01</date><risdate>2004</risdate><volume>36</volume><issue>7</issue><spage>732</spage><epage>737</epage><pages>732-737</pages><issn>1061-4036</issn><eissn>1546-1718</eissn><coden>NGENEC</coden><abstract>Hirschsprung disease (HSCR) is a multigenic, congenital disorder that affects 1 in 5,000 newborns and is characterized by the absence of neural crest-derived enteric ganglia in the colon. One of the primary genes affected in HSCR encodes the G protein-coupled endothelin receptor-B (EDNRB). The expression of Ednrb is required at a defined time period during the migration of the precursors of the enteric nervous system (ENS) into the colon. In this study, we describe a conserved spatiotemporal ENS enhancer of Ednrb. This 1-kb enhancer is activated as the ENS precursors approach the colon, and partial deletion of this enhancer at the endogenous Ednrb locus results in pigmented mice that die postnatally from megacolon. We identified binding sites for SOX10, an SRY-related transcription factor associated with HSCR, in the Ednrb ENS enhancer, and mutational analyses of these sites suggested that SOX10 may have multiple roles in regulating Ednrb in the ENS.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>15170213</pmid><doi>10.1038/ng1371</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Agriculture Animal Genetics and Genomics Animals Base Sequence Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Research Cell receptors Cell structures and functions Cloning Complications and side effects Diagnosis Enhancer Elements, Genetic Enteric Nervous System - physiology Fundamental and applied biological sciences. Psychology Gene expression Gene Expression Regulation - physiology Gene Function Gene mutations Genetic aspects Genetics of eukaryotes. Biological and molecular evolution Health aspects High Mobility Group Proteins - physiology Hirschsprung's disease Human Genetics letter Mice Mice, Transgenic Miscellaneous Molecular and cellular biology Molecular Sequence Data Mutation Neoplasm Proteins - physiology Receptors, Endothelin - genetics Risk factors Sequence Homology, Nucleic Acid SOXE Transcription Factors Transcription Factors |
| title | Spatiotemporal regulation of endothelin receptor-B by SOX10 in neural crest-derived enteric neuron precursors |
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