Rx is target of FGF8 signaling in the developing eye. It is first expressed in mouse embryos at during gastrulation in the presumptive forebrain and becomes restricted to the developing retina, posterior pituitary and hypothalamus. Deletion of the Rx gene revealed that it is required for the formation of these structures, as its loss causes anophthalmia and ventral neural tube defects. To determine the role of Rx later in eye development and in adult retina physiology, we have produced mice that carry a conditional Rx allele so that normal Rx function can be disrupted by Cre-mediated recombination. Inactivation of Rx in the developing optic vesicle causes two defects: the lens doesnt form and the optic vesicle forms retinal pigmented epithelium at the expense of neural retina. Our data supports a model in which Rx is required for Bmp4, Fgf8, and Fgf8/15 expression, which in turn is required for proper development of the eye.
| Waters, Samuel T; Wilson, Catherine P; Lewandoski, Mark (2003) Cloning and embryonic expression analysis of the mouse Gbx1 gene. Gene Expr Patterns 3:313-7 |
| Kim, Yong-Sik; Nakanishi, Gen; Lewandoski, Mark et al. (2003) GLIS3, a novel member of the GLIS subfamily of Kruppel-like zinc finger proteins with repressor and activation functions. Nucleic Acids Res 31:5513-25 |
