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Journal Article

Rescue of the tail defect of Brachyury mice

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Stott,  D
Department Biochemistry, Max Planck Institute for Developmental Biology, Max Planck Society;

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Kispert,  A       
Department Biochemistry, Max Planck Institute for Developmental Biology, Max Planck Society;

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Herrmann,  BG       
Department Biochemistry, Max Planck Institute for Developmental Biology, Max Planck Society;

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Citation

Stott, D., Kispert, A., & Herrmann, B. (1993). Rescue of the tail defect of Brachyury mice. Genes and Development, 7(2), 197-203. doi:10.1101/gad.7.2.197.


Cite as: https://hdl.handle.net/21.11116/0000-000D-A28D-D
Abstract
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.