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EMBO reports 4, 9, 894–899 (2003)
doi:10.1038/sj.embor.embor919
AOP Published online: 29 August 2003
Loss of eyes in zebrafish caused by mutation of chokh/rx3
Felix Loosli1, Wendy Staub2, Karin C. Finger-Baier2, Elke A. Ober3, Heather Verkade3, Joachim Wittbrodt1 & Herwig Baier2
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1 Developmental Biology Programme, European
Molecular Biology Laboratory, Meyerhofstrasse 1, PO Box
10.2209, 69012 Heidelberg,
Germany
2 Department of Physiology, Programs in Genetics,
Human Genetics, Neuroscience, and Developmental Biology, 513 Parnassus Avenue,
University of California, San Francisco, California
94143 0444, USA
3 Department of Biochemistry, Programs in Genetics,
Human Genetics, Neuroscience, and Developmental Biology, 513 Parnassus Avenue,
University of California, San Francisco, California
94143 0444, USA
To whom correspondence should be addressed
Herwig Baier Tel: +1 415 502 4301; Fax: +1 415 476 4929;
hbaier@itsa.ucsf.edu
Received 30 May 2003; Accepted 15 July 2003; Published online 29 August 2003.
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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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