Rescue of the tail defect of Brachyury mice.
The mouse Brachyury (T) gene is required for normal development of axial structures. Embryos homozygous for the T mutation show severe deficiencies in mesoderm formation. They lack the notochord and allantois, have abnormal somites, and die at approximately 10 days postcoitum probably as a result of the allantois defect. Mice heterozygous for the T mutation exhibit a variable short-tailed phenotype. The T gene has been cloned and shown to be expressed in the tissues most strongly affected by the mutation. In this paper, we show that a single-copy transgene representing the wild-type T allele is able to rescue the T-associated tail phenotype. In addition, we show that increasing dosage of the T gene in Tc/+ mice causes an increased extension of the axis. These data show the correlation of the level of T product with the extension of the anteroposterior axis, directly demonstrating the involvement of the T product in this process.
Stott
D
D
Max-Planck-Institut für Entwicklungsbiologie, Tübingen, Germany.
Kispert
A
A
Herrmann
B G
BG
D000482:Allantois / Q000002:abnormalities / Q000196:embryology*; D000818:Animals; D001483:Base Sequence; D003001:Cloning, Molecular; D004303:Dosage Compensation, Genetic; D051379:Mice; D008822:Mice, Transgenic; D008969:Molecular Sequence Data; D009154:Mutation / Q000235:genetics*; D009672:Notochord / Q000002:abnormalities / Q000196:embryology*; D010641:Phenotype; D013623:Tail / Q000002:abnormalities / Q000196:embryology*