Journal
INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY
Volume 48, Issue 8-9, Pages 761-770Publisher
UNIV BASQUE COUNTRY UPV-EHU PRESS
DOI: 10.1387/ijdb.041878tb
Keywords
retina; Rx; Rax; eye development
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Funding
- NEI NIH HHS [T32 EY07102, EY12505] Funding Source: Medline
- NATIONAL EYE INSTITUTE [T32EY007102, R01EY012505] Funding Source: NIH RePORTER
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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.
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