<i>Tbx20</i>is essential for cardiac chamber differentiation and repression of<i>Tbx2</i>

• Manvendra K. Singh

  Institut für Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany

• Vincent M. Christoffels

  Department of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands

• José M. Dias

  Department of Cell and Molecular Biology, Karolinska Institute, 17177 Stockholm, Sweden

• Mark-Oliver Trowe

  Institut für Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany

• Marianne Petry

  Institut für Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany

• Karin Schuster-Gossler

  Institut für Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany

• Antje Bürger

  Institut für Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany

• Johan Ericson

  Department of Cell and Molecular Biology, Karolinska Institute, 17177 Stockholm, Sweden

• Andreas Kispert

  Institut für Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany

抄録

Tbx20, a member of the T-box family of transcriptional regulators,shows evolutionary conserved expression in the developing heart. In the mouse, Tbx20 is expressed in the cardiac crescent, then in the endocardium and myocardium of the linear and looped heart tube before it is restricted to the atrioventricular canal and outflow tract in the multi-chambered heart. Here, we show that Tbx20 is required for progression from the linear heart tube to a multi-chambered heart. Mice carrying a targeted mutation of Tbx20 show early embryonic lethality due to hemodynamic failure. A linear heart tube with normal anteroposterior patterning is established in the mutant. The tube does not elongate, indicating a defect in recruitment of mesenchyme from the secondary heart field, even though markers of the secondary heart field are not affected. Furthermore, dorsoventral patterning of the tube, formation of working myocardium, looping, and further differentiation and morphogenesis fail. Instead, Tbx2, Bmp2and vinexin α (Sh3d4), genes normally restricted to regions of primary myocardium and lining endocardium, are ectopically expressed in the linear heart tube of Tbx20 mutant embryos. Because Tbx2 is both necessary and sufficient to repress chamber differentiation(Christoffels et al., 2004a; Harrelson et al., 2004), Tbx20 may ensure progression to a multi-chambered heart by repressing Tbx2 in the myocardial precursor cells of the linear heart tube destined to form the chambers.

収録刊行物

• Development

  Development 132 (12), 2697-2707, 2005-06-15

  The Company of Biologists

キーワード

• Developmental Biology
• Molecular Biology

詳細情報

• CRID: 1361418520000401024
• NII論文ID: 30002334593
• DOI: 10.1242/dev.01854
• ISSN: 14779129
• ISSN: 09501991
• Web Site: http://journals.biologists.com/dev/article-pdf/132/12/2697/1508698/2697.pdf
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