Int. J. Dev. Biol. 48: 761 - 770 (2004)
doi: 10.1387/ijdb.041878tb
© UBC Press

Regulation of vertebrate eye development by Rx genes

Travis J. Bailey1, Heithem El-Hodiri3, Li Zhang4, Rina Shah2, Peter H. Mathers5 and Milan Jamrich*,1,2

1Program in Developmental Biology, Baylor College of Medicine, Houston, TX, USA, 2Departments of Molecular and Human Genetics and Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA, 3Division of Molecular and Human Genetics, Children's Research Institute, Columbus, OH, USA, 4Novasite Pharmaceuticals, Inc., San Diego, CA, USA and 5Sensory Neuroscience Research Center, West Virginia University School of Medicine, Morgantown, WV, USA

ABSTRACT The paired-like homeobox-containing gene Rx has a critical role in the eye development of several vertebrate species including Xenopus, mouse, chicken, medaka, zebrafish and human. Rx is initially expressed in the anterior neural region of developing embryos, and later in the retina and ventral hypothalamus. Abnormal regulation or function of Rx results in severe abnormalities of eye formation. Overexpression of Rx in Xenopus and zebrafish embryos leads to overproliferation of retinal cells. A targeted elimination of Rx in mice results in a lack of eye formation. Mutations in Rx genes are the cause of the mouse mutation eyeless (ey1), the medaka temperature sensitive mutation eyeless (el) and the zebrafish mutation chokh. In humans, mutations in Rx lead to anophthalmia. All of these studies indicate that Rx genes are key factors in vertebrate eye formation. Because these results cannot be easily reconciled with the most popular dogmas of the field, we offer our interpretation of eye development and evolution.

Keywords:

retina, Rx, Rax, eye development

*Corresponding author e-mail: jamrich@bcm.tmc.edu