LymphedemaV1, Main, Exploration, bibRecord, 008F54

Tbx1 is regulated by tissue-specific forkhead proteins through a common Sonic hedgehog-responsive enhancer

Identifieur interne : 008F54 ( Main/Exploration ); précédent : 008F53; suivant : 008F55

Tbx1 is regulated by tissue-specific forkhead proteins through a common Sonic hedgehog-responsive enhancer

Auteurs : Hiroyuki Yamagishi [États-Unis] ; Jun Maeda [États-Unis] ; Tonghuan Hu [États-Unis] ; John Mcanally [États-Unis] ; Simon J. Conway [États-Unis] ; Tsutomu Kume [États-Unis] ; Erik N. Meyers [États-Unis] ; Chihiro Yamagishi [États-Unis] ; Deepak Srivastava [États-Unis]

Source :

Genes & Development [ 0890-9369 ] ; 2003.

RBID : PMC:195981

Abstract

Haploinsufficiency of Tbx1 is likely a major determinant of cardiac and craniofacial birth defects associated with DiGeorge syndrome. Although mice deficient in Tbx1 exhibit pharyngeal and aortic arch defects, the developmental program and mechanisms through which Tbx1 functions are relatively unknown. We identified a single cis-element upstream of Tbx1 that recognized winged helix/forkhead box (Fox)-containing transcription factors and was essential for regulation of Tbx1 transcription in the pharyngeal endoderm and head mesenchyme. The Tbx1 regulatory region was responsive to signaling by Sonic hedgehog (Shh) in vivo. We show that Shh is necessary for aortic arch development, similar to Tbx1, and is also required for expression of Foxa2 and Foxc2 in the pharyngeal endoderm and head mesenchyme, respectively. Foxa2, Foxc1, or Foxc2 could bind and activate transcription through the critical cis-element upstream of Tbx1, and Foxc proteins were required, within their expression domains, for Tbx1 transcription in vivo. We propose that Tbx1 is a direct transcriptional target of Fox proteins and that Fox proteins may serve an intermediary role in Shh regulation of Tbx1.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC195981

DOI: 10.1101/gad.1048903
PubMed: 12533514
PubMed Central: 195981

Affiliations:

États-Unis

Le document en format XML

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<front><div type="abstract" xml:lang="en"><p>Haploinsufficiency of Tbx1 is likely a major determinant of cardiac and craniofacial birth defects associated with DiGeorge syndrome. Although mice deficient in Tbx1 exhibit pharyngeal and aortic arch defects, the developmental program and mechanisms through which Tbx1 functions are relatively unknown. We identified a single <italic>cis</italic>
-element upstream of <italic>Tbx1</italic>
 that recognized winged helix/forkhead box (Fox)-containing transcription factors and was essential for regulation of <italic>Tbx1</italic>
 transcription in the pharyngeal endoderm and head mesenchyme. The <italic>Tbx1</italic>
 regulatory region was responsive to signaling by Sonic hedgehog (Shh) in vivo. We show that Shh is necessary for aortic arch development, similar to Tbx1, and is also required for expression of <italic>Foxa2</italic>
 and <italic>Foxc2</italic>
 in the pharyngeal endoderm and head mesenchyme, respectively. Foxa2, Foxc1, or Foxc2 could bind and activate transcription through the critical <italic>cis</italic>
-element upstream of <italic>Tbx1</italic>
, and Foxc proteins were required, within their expression domains, for <italic>Tbx1</italic>
 transcription in vivo. We propose that <italic>Tbx1</italic>
 is a direct transcriptional target of Fox proteins and that Fox proteins may serve an intermediary role in Shh regulation of <italic>Tbx1</italic>
.</p>
</div>
</front>
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Serveur d'exploration sur le lymphœdème

Tbx1 is regulated by tissue-specific forkhead proteins through a common Sonic hedgehog-responsive enhancer

Tbx1 is regulated by tissue-specific forkhead proteins through a common Sonic hedgehog-responsive enhancer

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Abstract

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