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Cold Spring Harbor Laboratory Press, Genes & Development, 11(15), p. 1427-1434, 2001

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

Journal article published in 2001 by Corinne Houart, Masaya Take-Uchi, Carl-Philipp Heisenberg, Gerd-Jörg Rauch, Neville Young, Pedro Coutinho, Ichiro Masai, Luca Caneparo, Miguel L. Concha, Stephen W. Wilson, Robert Geisler, Trevor Clive Dale ORCID, Derek L. Stemple
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

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 Gsk3β 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.