Loss of eyes in zebrafish caused by mutation of chokh/rx3
- Loosli, F., Staub, W., Finger-Baier, K.C., Ober, E.A., Verkade, H., Wittbrodt, J., and Baier, H.
- EMBO reports 4(9): 894-899 (Journal)
- Registered Authors
- Baier, Herwig, Finger-Baier, Karin, Loosli, Felix, Ober, Elke, Staub, Wendy, Verkade, Heather, Wittbrodt, Jochen
- MeSH Terms
- Eye Abnormalities/genetics*
- Eye Proteins
- Fish Proteins/genetics*
- Homeodomain Proteins/biosynthesis
- Homeodomain Proteins/genetics*
- Nerve Tissue Proteins/biosynthesis
- Nerve Tissue Proteins/genetics
- Paired Box Transcription Factors
- Point Mutation
- Repressor Proteins
- Zebrafish Proteins/biosynthesis
- Zebrafish Proteins/genetics
- 12947416 Full text @ EMBO Rep.
Loosli, F., Staub, W., Finger-Baier, K.C., Ober, E.A., Verkade, H., Wittbrodt, J., and Baier, H. (2003) Loss of eyes in zebrafish caused by mutation of chokh/rx3. EMBO reports. 4(9):894-899.
The vertebrate eye forms by specification of the retina anlage and subsequent morphogenesis of the optic vesicles, from which the neural retina differentiates. chokh (chk) mutant zebrafish lack eyes from the earliest stages in development. Marker gene analysis indicates that retinal fate is specified normally, but optic vesicle evagination and neuronal differentiation are blocked. We show that the chk gene encodes the homeodomain-containing transcription factor, Rx3. Loss of Rx3 function in another teleost, medaka, has also been shown to result in an eyeless phenotype. The medaka rx3 locus can fully rescue the zebrafish mutant phenotype. We provide evidence that the regulation of rx3 is evolutionarily conserved, whereas the downstream cascade contains significant differences in gene regulation. Thus, these mutations in orthologous genes allow us to study the evolution of vertebrate eye development at the molecular level.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes