INACTIVATION OF THE ZEBRAFISH HOMOLOG OF CHX10 BY ANTISENSE OLIGONUCLEOTIDES CAUSES EYE MALFORMATIONS SIMILAR TO THE OCULAR RETARDATION PHENOTYPE

Citation
Sml. Barabino et al., INACTIVATION OF THE ZEBRAFISH HOMOLOG OF CHX10 BY ANTISENSE OLIGONUCLEOTIDES CAUSES EYE MALFORMATIONS SIMILAR TO THE OCULAR RETARDATION PHENOTYPE, Mechanisms of development, 63(2), 1997, pp. 133-143
Citations number
34
Categorie Soggetti
Developmental Biology
Journal title
ISSN journal
09254773
Volume
63
Issue
2
Year of publication
1997
Pages
133 - 143
Database
ISI
SICI code
0925-4773(1997)63:2<133:IOTZHO>2.0.ZU;2-F
Abstract
We report the cloning of a zebrafish paired-type homeobox gene, Air, c losely related to the murine Chx10 and the gold fish Vsx-1 homeodomain proteins. Air is first expressed at about 12 h post-fertilization (hp f) when optic vesicles appear. Its expression is restricted to the ear ly retinal neuroepithelium, whereas no signal can be detected in the o ptic placode. Later, Alx expression follows the differentiation of the neural retina. Inhibition experiments with antisense oligonucleotides resulted in specific eye malformations which are reminiscent of the p henotype of ocular retardation (or) mice, caused by a spontaneous Chx1 0 mutation. The expression of other developmentally relevant genes suc h as pax(zf-a), pax(zf-b) and krx-20 was not affected in the antisense treated embryos. (C) 1997 Elsevier Science Ireland Ltd.