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First published online 18 May 2005
doi: 10.1242/dev.01854
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1 Institut für Molekularbiologie, Medizinische Hochschule Hannover, 30625
Hannover, Germany
2 Department of Anatomy and Embryology, Academic Medical Center, University of
Amsterdam, 1105 AZ Amsterdam, The Netherlands
3 Department of Cell and Molecular Biology, Karolinska Institute, 17177
Stockholm, Sweden
* Author for correspondence (e-mail: kispert.andreas{at}mh-hannover.de)
Accepted 6 April 2005
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, Bmp2
and vinexin 
(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.
Key words: T-box, Heart, Myocardium, Anterior heart field, Bmp
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