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Tbx1 is Regulated by Forkhead Proteins in the Secondary Heart Field

Identifieur interne : 007A64 ( Main/Exploration ); précédent : 007A63; suivant : 007A65

Tbx1 is Regulated by Forkhead Proteins in the Secondary Heart Field

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.

RBID : PMC:3316489

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 Tbx1 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 Tbx1 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 Tbx1 enhancer suggests that SHF-derived Tbx1-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, Tbx1 expression domains, and that Tbx1 marks a subset of SHF-derived cells, particularly those that uniquely contribute to the right-sided outflow tract and proximal pulmonary artery.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3316489

DOI: 10.1002/dvdy.20686
PubMed: 16444712
PubMed Central: 3316489

Affiliations:

Le document en format XML

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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>
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Tbx1 is Regulated by Forkhead Proteins in the Secondary Heart Field

Tbx1 is Regulated by Forkhead Proteins in the Secondary Heart Field

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