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H. Wang, J. Kesinger, Y. Tang, B. Frank, M. Centola; Altered Gene Expression in a Zebrafish Eyeless Mutant (mbl/axin1) . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3125.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:The suppression of Wnt signaling in the canonical pathway is shown to de–repress a cascade of target genes, some of which are implicated to be able to induce the formation of the brain and the eyes. Both the brain and the eyes, particularly the retina, are thought to be autonomous circadian oscillators and many canonical circadian clock genes are rhythmically expressed in the brain and the eyes in a robust fashion in zebrafish (Danio rerio). Yet, little is known about how Wnt signaling regulates circadian rhythmicity and the presumable Wnt signaling target genes that may control daily oscillations of the circadian clock genes. Masterblind (mbl) is an ethyl nitrosourea (ENU)–induced mutant generated in a large–scale zebrafish mutagenesis. Zebrafish embryos homozygous for the masterblind (mbl–/–) mutation exhibit reduced or absent eyes and telecephalon, and the expansion of the diencephalic fates to the front of the brain. A mutation in the GSK3–binding domain of zebrafish axin1, encoding a scaffolding protein in the Wnt signaling pathway, results in the mbl phenotype. Methods:We employ 14000–oligonucleotide zebrafish gene chips to profile gene expression in mutant (mbl–/–) and wild type control embryos. Results/Conclusions: A number of differentially expressed genes identified by microarray analysis, whose expression levels are further confirmed by independent in situ hybridization or real–time PCR, could be target genes that directly lead to the mbl phenotype and may represent possible links between Wnt signaling and circadian oscilation.
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