Tbx1 is Regulated by Forkhead Proteins in the Secondary Heart Field
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Auteurs : Jun Maeda [Japon, États-Unis] ; Hiroyuki Yamagishi [Japon, États-Unis] ; John Mcanally [États-Unis] ; Chihiro Yamagisihi [Japon, États-Unis] ; Deepak Srivastava [États-Unis]Source :
- Developmental Dynamics [ 1058-8388 ] ; 2006.
Abstract
Transcriptional regulation in a tissue-specific and quantitative fashion is essential for developmental events, including those involved in cardiovascular morphogenesis. Tbx1 is a T-box containing transcription factor that is responsible for many of the defects observed in 22q11 deletion syndrome in humans. Tbx1 is expressed in the secondary heart field (SHF) and is essential for cardiac outflow tract (OFT) development. We previously reported that
Url:
DOI: 10.1002/dvdy.20686
PubMed: 16444712
PubMed Central: 3316489
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<front><div type="abstract" xml:lang="en"><p id="P2">Transcriptional regulation in a tissue-specific and quantitative fashion is essential for developmental events, including those involved in cardiovascular morphogenesis. Tbx1 is a T-box containing transcription factor that is responsible for many of the defects observed in 22q11 deletion syndrome in humans. Tbx1 is expressed in the secondary heart field (SHF) and is essential for cardiac outflow tract (OFT) development. We previously reported that <italic>Tbx1</italic>
is regulated by sonic hedgehog via forkhead (Fox) transcription factors in the head mesenchyme and pharyngeal endoderm, but how it is regulated in the SHF is unknown. Here, we show that <italic>Tbx1</italic>
expression in the SHF is regulated by Fox proteins through a combination of two evolutionally conserved Fox binding sites in a dose-dependent manner. Cell fate analyses using the <italic>Tbx1</italic>
enhancer suggests that SHF-derived <italic>Tbx1</italic>
-expressing cells contribute extensively to the right ventricular myocardium as well as the OFT during early development and ultimately give rise to the right ventricular infundibulum, pulmonary trunk and pulmonary valves. These results suggest that Fox proteins are involved in most, if not all, <italic>Tbx1</italic>
expression domains, and that <italic>Tbx1</italic>
marks a subset of SHF-derived cells, particularly those that uniquely contribute to the right-sided outflow tract and proximal pulmonary artery.</p>
</div>
</front>
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<pmc article-type="research-article" xml:lang="en"><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">9201927</journal-id>
<journal-id journal-id-type="pubmed-jr-id">1281</journal-id>
<journal-id journal-id-type="nlm-ta">Dev Dyn</journal-id>
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<journal-title-group><journal-title>Developmental Dynamics</journal-title>
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<article-id pub-id-type="manuscript">NIHMS69987</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
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<title-group><article-title><italic>Tbx1</italic>
is Regulated by Forkhead Proteins in the Secondary Heart Field</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Maeda</surname>
<given-names>Jun</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
<xref ref-type="author-notes" rid="FN1">*</xref>
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<contrib contrib-type="author"><name><surname>Yamagishi</surname>
<given-names>Hiroyuki</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
<xref ref-type="author-notes" rid="FN1">*</xref>
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<contrib contrib-type="author"><name><surname>McAnally</surname>
<given-names>John</given-names>
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<xref ref-type="aff" rid="A2">2</xref>
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<contrib contrib-type="author"><name><surname>Yamagisihi</surname>
<given-names>Chihiro</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Srivastava</surname>
<given-names>Deepak</given-names>
</name>
<xref ref-type="aff" rid="A2">2</xref>
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</contrib-group>
<aff id="A1"><label>1</label>
Department of Pediatrics, Division of Pediatric Cardiology, Keio University School of Medicine, Tokyo, Japan</aff>
<aff id="A2"><label>2</label>
Department of Pediatrics and Molecular Biology, University of Texas Southwestern Medical Center, TX</aff>
<author-notes><corresp id="cor1">Corresponding to: Deepak Srivastava, Present Address (Address for correspondence): Gladstone Institute of Cardiovascular Disease and Department of Pediatrics, University of California San Francisco, 1650 Owens Street, San Francisco, CA 94158, Ph: 415-734-2716, Fax: 415-734-0141, <email>dsrivastava@gladstone.ucsf.edu</email>
</corresp>
<corresp id="cor2">Designated alternate corresponding author: Jun Maeda, Hiroyuki Yamagishi, Address for alternate correspondence: Department of Pediatrics, Keio University School of Medicine, 35 Shinanomachi, Shinjyuku-ku, Tokyo 160-8582, Japan, Ph: +81-3-3353-1221 (ext 62365), Fax: +81-3-5379-1978, <email>jmaeda@1991.jukuin.keio.ac.jp</email>
(JM), <email>hyamag@sc.itc.keio.ac.jp</email>
(HY)</corresp>
<fn id="FN1" fn-type="equal"><label>*</label>
<p id="P1">These authors contributed equally to this work.</p>
</fn>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>20</day>
<month>3</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="ppub"><month>3</month>
<year>2006</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>30</day>
<month>3</month>
<year>2012</year>
</pub-date>
<volume>235</volume>
<issue>3</issue>
<fpage>701</fpage>
<lpage>710</lpage>
<abstract><p id="P2">Transcriptional regulation in a tissue-specific and quantitative fashion is essential for developmental events, including those involved in cardiovascular morphogenesis. Tbx1 is a T-box containing transcription factor that is responsible for many of the defects observed in 22q11 deletion syndrome in humans. Tbx1 is expressed in the secondary heart field (SHF) and is essential for cardiac outflow tract (OFT) development. We previously reported that <italic>Tbx1</italic>
is regulated by sonic hedgehog via forkhead (Fox) transcription factors in the head mesenchyme and pharyngeal endoderm, but how it is regulated in the SHF is unknown. Here, we show that <italic>Tbx1</italic>
expression in the SHF is regulated by Fox proteins through a combination of two evolutionally conserved Fox binding sites in a dose-dependent manner. Cell fate analyses using the <italic>Tbx1</italic>
enhancer suggests that SHF-derived <italic>Tbx1</italic>
-expressing cells contribute extensively to the right ventricular myocardium as well as the OFT during early development and ultimately give rise to the right ventricular infundibulum, pulmonary trunk and pulmonary valves. These results suggest that Fox proteins are involved in most, if not all, <italic>Tbx1</italic>
expression domains, and that <italic>Tbx1</italic>
marks a subset of SHF-derived cells, particularly those that uniquely contribute to the right-sided outflow tract and proximal pulmonary artery.</p>
</abstract>
<kwd-group><kwd>Tbx1</kwd>
<kwd>secondary heart field</kwd>
<kwd>Fox proteins</kwd>
<kwd>cardiac outflow tract</kwd>
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<funding-group><award-group><funding-source country="United States">National Heart, Lung, and Blood Institute : NHLBI</funding-source>
<award-id>U01 HL100406-04 || HL</award-id>
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<award-group><funding-source country="United States">National Heart, Lung, and Blood Institute : NHLBI</funding-source>
<award-id>R24 HL092851-04 || HL</award-id>
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<award-group><funding-source country="United States">National Heart, Lung, and Blood Institute : NHLBI</funding-source>
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<award-group><funding-source country="United States">National Heart, Lung, and Blood Institute : NHLBI</funding-source>
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</front>
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