A mutation in the Gsk3-binding domain of zebrafish Masterblind/Axin1 leads to a 
fate transformation of telencephalon and eyes to diencephalon

Heisenberg, C-P; Houart, C; Take-uchi , M; Rauch, G-J; Young, N; Coutinho, P; Masai, I; Caneparo , L; Concha, ML; Geisler, R; Dale, CT; Wilson, SW; Stemple, DL

doi:10.1101/gad.194301

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A mutation in the Gsk3-binding domain of zebrafish Masterblind/Axin1 leads to a fate transformation of telencephalon and eyes to diencephalon

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Rauch, G-J
Department Genetics, Max Planck Institute for Developmental Biology, Max Planck Society;

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Geisler, R
Department Genetics, Max Planck Institute for Developmental Biology, Max Planck Society;

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引用

Heisenberg, C.-P., Houart, C., Take-uchi, M., Rauch, G.-J., Young, N., Coutinho, P., Masai, I., Caneparo, L., Concha, M., Geisler, R., Dale, C., Wilson, S., & Stemple, D. (2001). A mutation in the Gsk3-binding domain of zebrafish Masterblind/Axin1 leads to a fate transformation of telencephalon and eyes to diencephalon. Genes and Development, 15(11), 1427-1434. doi:10.1101/gad.194301.

引用: https://hdl.handle.net/21.11116/0000-000D-65F4-E

要旨

Zebrafish embryos homozygous for the masterblind (mbl) mutation exhibit a striking phenotype in which the eyes and telencephalon are reduced or absent and diencephalic fates expand to the front of the brain. Here we show that mbl(-/-) embryos carry an amino-acid change at a conserved site in the Wnt pathway scaffolding protein, Axin1. The amino-acid substitution present in the mbl allele abolishes the binding of Axin to Gsk3 and affects Tcf-dependent transcription. Therefore, Gsk3 activity may be decreased in mbl(-/-) embryos and in support of this possibility, overexpression of either wild-type Axin1 or Gsk3beta can restore eye and telencephalic fates to mbl(-/-) embryos. Our data reveal a crucial role for Axin1-dependent inhibition of the Wnt pathway in the early regional subdivision of the anterior neural plate into telencephalic, diencephalic, and eye-forming territories.