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First published online 7 March 2007
doi: 10.1242/dev.000117


Development 134, 1455-1463 (2007)
Published by The Company of Biologists 2007


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Foxe view of lens development and disease

Olga Medina-Martinez and Milan Jamrich*

Department of Molecular and Cellular Biology, and Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.


Figure 1
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Fig. 1. Schematic of vertebrate lens development. (A) Morphogenesis of the lens begins when the evaginating optic vesicle (OV), which derives from the neuroectoderm (NE, blue), contacts the head surface ectoderm (HSE, yellow). (B) Upon this contact, the HSE thickens and forms a lens placode (LP). (C,D) The optic cup subsequently forms the retina (R) and the lens placode invaginates and forms a lens vesicle (LV). (E) Once the vesicle is formed, the lens cells in the posterior half of the vesicle elongate and form the lens fiber cells (LF). By contrast, the cells in the anterior of the lens vesicle remain as a monolayer and form the anterior lens epithelium (ALE). Modified with permission from Lovicu and McAvoy (Lovicu and McAvoy, 2005Go).

 

Figure 2
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Fig. 2. A comparison of wild-type and Foxe3 mutant mouse eyes. (A) Hematoxylin-Eosin (HE)-stained coronal section of a P14 wild-type mouse eye showing a lens stained in pink. (B) An HE-stained coronal section of a P1 eye from a dyl mouse showing an abnormal small lens, cornea and retina (blue). (C,D) Coronal sections of eyes from P14 Foxe3-/- mice showing abnormal features of the lens, cornea and retina. Note the rudimentary lens (arrowed) in D. (E) Cerebral magnetic resonance imaging (MRI) of a 3-year-old human subject with a mutated FOXE3 gene, showing absence of the lens. (F) An HE-stained section through the eye of a 3-month-old child with a mutated FOXE3 gene, showing the absence of the lens (arrow). The asterisk indicates the empty cavity, most likely corresponding to the vitreous. c, cornea; l, lens; on, optic nerve; r, retina. A,C,D are reproduced with permission from Medina-Martinez et al. (Medina-Martinez et al., 2005Go); B is from I. Brownell and M.J., unpublished; E,F are reproduced with permission from Valleix et al. (Valleix et al., 2006Go).

 

Figure 3
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Fig. 3. Regulatory interactions during lens formation in the head surface ectoderm and lens. (A) Schematic depicting selected transcription factors important for lens formation that are expressed in the mouse head surface ectoderm. These interactions help specify the activation of Foxe3 in the lens placode. (B) Roles of Foxe3 in the development and differentiation of the lens (orange). Feedback loops are not depicted here and arrows between genes do not necessarily imply direct regulatory interactions.

 

Figure 4
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Fig. 4. Expression of Xlens1 and Foxe3 during lens formation in Xenopus and mouse. (A) Anterior view of Xlens1 expression in the U-shaped region of Xenopus neurula (our unpublished observation). (B) Expression of Xlens1 in the lens placodes of a Xenopus tadpole (Kenyon et al., 1999Go). (C) The earliest expression of Foxe3 in the lens placode of an E9.0 mouse embryos (arrow). Reproduced with permission from Blixt et al. (Blixt et al., 2000Go). (D) Expression of Foxe3 in an E12 mouse embryo. Reproduced with permission from Brownell et al. (Brownell et al., 2000Go).

 





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