Int. J. Dev. Biol. 48: 761 - 770 (2004)

https://doi.org/10.1387/ijdb.041878tb

Vol 48, Issue 8-9

Special Issue: Eye Development

Regulation of vertebrate eye development by Rx genes

Published: 1 November 2004

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