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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>
<pmc-dir>properties manuscript</pmc-dir>
<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>
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