Figure 3.

Compound ocular anomalies in Tgfbr2-mutant mice. (a) Toluidine blue staining of semi-thin sagittal sections of eyes at E18 reveals a smaller size with no anterior chamber and an infiltration of cells behind the lens in Tgfbr2-mutant embryos as compared with control embryos. Boxes indicate magnified regions shown in the other panels; scale bars represent 250 μm. (b) Abnormal corneal stroma in Tgfbr2-mutant embryos. (c) Structures of the forming chamber angle, including the trabecular meshwork (black arrowhead) in control eyes are absent in Tgfbr2-mutant eyes (open black arrowhead). Here, the lens and the cornea fail to separate to form the anterior eye chamber (open arrow). In addition, dark-field images (insets) visualizing the pigment of the forming iris (broken line in the main image) reveal initiation of ciliary-body formation (white arrowheads) in control eyes and its absence in Tgfbr2-mutant eyes (open white arrowheads). (d) In control eyes, the primary vitreous consists of loosely arranged vessels of the hyaloid vascular system (arrows). In contrast, Tgfbr2-mutant mice show a dense cell mass between the lens and the retina (asterisk), reminiscent of human persistent hyperplastic primary vitreous. (e) The retina of control eyes displays typical patterning, with clear separation into an inner layer (IRL) and an outer layer (ORL). In Tgfbr2-mutant mice, however, there is no apparent patterning of the retina.

Ittner et al. Journal of Biology 2005 4:11   doi:10.1186/jbiol29
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