AI Article Synopsis
- The vertebrate eye develops from the retina anlage and optic vesicles, where the neural retina forms.
- Chokh (chk) mutant zebrafish lack eyes early in development due to blocked optic vesicle formation and neuronal differentiation, despite normal retinal fate specification.
- The chk gene is identified as the transcription factor Rx3, which, when mutated, leads to an eyeless condition in both zebrafish and medaka, indicating evolutionary conservation in gene regulation but differences in downstream processes.
Article Abstract
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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1326357 | PMC |
| http://dx.doi.org/10.1038/sj.embor.embor919 | DOI Listing |
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