Article

Formation of multiple hearts in mice following deletion of beta-catenin in the embryonic endoderm.

Department of Molecular Embryology, Max-Planck Institute for Immunobiology, Stuebeweg 51, D-79108 Freiburg, Germany.
Developmental Cell (impact factor: 14.03). 09/2002; 3(2):171-81.
Source: PubMed

ABSTRACT Using Cre/loxP, we conditionally inactivated the beta-catenin gene in cells of structures that exhibit important embryonic organizer functions: the visceral endoderm, the node, the notochord, and the definitive endoderm. Mesoderm formation was not affected in the mutant embryos, but the node was missing, patterning of the head and trunk was affected, and no notochord or somites were formed. Surprisingly, deletion of beta-catenin in the definitive endoderm led to the formation of multiple hearts all along the anterior-posterior (A/P) axis of the embryo. Ectopic hearts developed in parallel with the normal heart in regions of ectopic Bmp2 expression. We provide evidence that ablation of beta-catenin in embryonic endoderm changes cell fate from endoderm to precardiac mesoderm, consistent with the existence of bipotential mesendodermal progenitors in mouse embryos.

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Keywords

ablation
 
bipotential mesendodermal progenitors
 
Cre/loxP
 
definitive endoderm
 
deletion
 
ectopic Bmp2 expression
 
Ectopic hearts
 
embryo
 
embryonic endoderm changes cell fate
 
embryonic organizer functions
 
endoderm
 
Mesoderm formation
 
mouse embryos
 
mutant embryos
 
normal heart
 
notochord
 
patterning
 
precardiac mesoderm
 
visceral endoderm