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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en"><italic>Etsrp/etv2</italic> is directly regulated by <italic>foxc1a/b</italic> in the zebrafish angioblast</title><author><name sortKey="Veldman, Matthew B" sort="Veldman, Matthew B" uniqKey="Veldman M" first="Matthew B." last="Veldman">Matthew B. Veldman</name></author><author><name sortKey="Lin, Shuo" sort="Lin, Shuo" uniqKey="Lin S" first="Shuo" last="Lin">Shuo Lin</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22135404</idno><idno type="pmc">3457812</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3457812</idno><idno type="RBID">PMC:3457812</idno><idno type="doi">10.1161/CIRCRESAHA.111.251298</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">003235</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003235</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main"><italic>Etsrp/etv2</italic> is directly regulated by <italic>foxc1a/b</italic> in the zebrafish angioblast</title><author><name sortKey="Veldman, Matthew B" sort="Veldman, Matthew B" uniqKey="Veldman M" first="Matthew B." last="Veldman">Matthew B. Veldman</name></author><author><name sortKey="Lin, Shuo" sort="Lin, Shuo" uniqKey="Lin S" first="Shuo" last="Lin">Shuo Lin</name></author></analytic><series><title level="j">Circulation research</title><idno type="ISSN">0009-7330</idno><idno type="eISSN">1524-4571</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Rationale</title><p id="P1">Endothelial cells are developmentally derived from angioblasts specified in the mesodermal germ cell layer. The transcription factor <italic>etsrp/etv2</italic> is at the top of the known genetic hierarchy for angioblast development. The transcriptional events that induce <italic>etsrp</italic> expression and angioblast specification are not well understood.</p></sec><sec id="S2"><title>Objective</title><p id="P2">We generated <italic>etsrp:gfp</italic> transgenic zebrafish and used them to identify regulatory regions and transcription factors critical for <italic>etsrp</italic> expression and angioblast specification from mesoderm.</p></sec><sec id="S3"><title>Methods and Results</title><p id="P3">To investigate the mechanisms that initiate angioblast cell transcription during embryogenesis, we have performed promoter analysis of the <italic>etsrp</italic> locus in zebrafish. We describe three enhancer elements sufficient for endothelial gene expression when place in front of a heterologous promoter. The deletion of all three regulatory regions led to a near complete loss of endothelial expression from the <italic>etsrp</italic> promoter. One of the enhancers, located 2.3 kb upstream of <italic>etsrp</italic> contains a consensus FOX binding site that binds Foxc1a and Foxc1b in vitro by EMSA and in vivo using ChIP. Combined knockdown of <italic>foxc1a</italic>/<italic>b</italic>, using morpholinos, led to a significant decrease in <italic>etsrp</italic> expression at early developmental stages as measured by quantitative RT-PCR and in situ hybridization. Decreased expression of primitive erythrocyte genes <italic>scl</italic> and <italic>gata1</italic> was also observed while pronephric gene <italic>pax2a</italic> was relatively normal in expression level and pattern.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">These findings identify mesodermal <italic>foxc1a/b</italic> as a direct upstream regulator of <italic>etsrp</italic> in angioblasts. This establishes a new molecular link in the process of mesoderm specification into angioblast.</p></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
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<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0047103</journal-id><journal-id journal-id-type="pubmed-jr-id">2974</journal-id><journal-id journal-id-type="nlm-ta">Circ Res</journal-id><journal-id journal-id-type="iso-abbrev">Circ. Res.</journal-id><journal-title-group><journal-title>Circulation research</journal-title></journal-title-group><issn pub-type="ppub">0009-7330</issn><issn pub-type="epub">1524-4571</issn></journal-meta><article-meta><article-id pub-id-type="pmid">22135404</article-id><article-id pub-id-type="pmc">3457812</article-id><article-id pub-id-type="doi">10.1161/CIRCRESAHA.111.251298</article-id><article-id pub-id-type="manuscript">NIHMS346284</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title><italic>Etsrp/etv2</italic> is directly regulated by <italic>foxc1a/b</italic> in the zebrafish angioblast</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Veldman</surname><given-names>Matthew B.</given-names></name><degrees>Ph.D.</degrees></contrib><contrib contrib-type="author"><name><surname>Lin</surname><given-names>Shuo</given-names></name><degrees>Ph.D.</degrees></contrib><aff id="A1">Department of Molecular, Cellular, and Developmental Biology, University of California-Los Angeles, CA, USA</aff></contrib-group><author-notes><corresp id="CR1">Corresponding author: Shuo Lin, Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, 621 Charles E. Young Drive South, Los Angeles, CA 90095-1606, <email>shuolin@ucla.edu</email>., Fax: 310-267-4971, Telephone: 310-267-4970</corresp></author-notes><pub-date pub-type="nihms-submitted"><day>10</day><month>9</month><year>2012</year></pub-date><pub-date pub-type="epub"><day>01</day><month>12</month><year>2011</year></pub-date><pub-date pub-type="ppub"><day>20</day><month>1</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>20</day><month>1</month><year>2013</year></pub-date><volume>110</volume><issue>2</issue><fpage>220</fpage><lpage>229</lpage><abstract><sec id="S1"><title>Rationale</title><p id="P1">Endothelial cells are developmentally derived from angioblasts specified in the mesodermal germ cell layer. The transcription factor <italic>etsrp/etv2</italic> is at the top of the known genetic hierarchy for angioblast development. The transcriptional events that induce <italic>etsrp</italic> expression and angioblast specification are not well understood.</p></sec><sec id="S2"><title>Objective</title><p id="P2">We generated <italic>etsrp:gfp</italic> transgenic zebrafish and used them to identify regulatory regions and transcription factors critical for <italic>etsrp</italic> expression and angioblast specification from mesoderm.</p></sec><sec id="S3"><title>Methods and Results</title><p id="P3">To investigate the mechanisms that initiate angioblast cell transcription during embryogenesis, we have performed promoter analysis of the <italic>etsrp</italic> locus in zebrafish. We describe three enhancer elements sufficient for endothelial gene expression when place in front of a heterologous promoter. The deletion of all three regulatory regions led to a near complete loss of endothelial expression from the <italic>etsrp</italic> promoter. One of the enhancers, located 2.3 kb upstream of <italic>etsrp</italic> contains a consensus FOX binding site that binds Foxc1a and Foxc1b in vitro by EMSA and in vivo using ChIP. Combined knockdown of <italic>foxc1a</italic>/<italic>b</italic>, using morpholinos, led to a significant decrease in <italic>etsrp</italic> expression at early developmental stages as measured by quantitative RT-PCR and in situ hybridization. Decreased expression of primitive erythrocyte genes <italic>scl</italic> and <italic>gata1</italic> was also observed while pronephric gene <italic>pax2a</italic> was relatively normal in expression level and pattern.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">These findings identify mesodermal <italic>foxc1a/b</italic> as a direct upstream regulator of <italic>etsrp</italic> in angioblasts. This establishes a new molecular link in the process of mesoderm specification into angioblast.</p></sec></abstract><kwd-group><kwd>angioblast</kwd><kwd><italic>etsrp</italic></kwd><kwd><italic>foxc1a</italic></kwd><kwd><italic>scl</italic></kwd><kwd>zebrafish</kwd></kwd-group><funding-group><award-group><funding-source country="United States">National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK</funding-source><award-id>R01 DK054508 || DK</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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