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Figure 3 | BMC Ophthalmology

Figure 3

From: αA-crystallin R49Cneomutation influences the architecture of lens fiber cell membranes and causes posterior and nuclear cataracts in mice

Figure 3

Lens phenotypes in R49C neo mice. (A-D) Eyes were dilated and examined by slit lamp. (A) Wild type mice (5 months old) had clear lenses (stage 0). (B) Heterozygous WT/R49Cneo αA-crystallin knock-in mice (3 months old) had opacity in the posterior and nuclear regions of the lens (stage 2). (C) Homozygous R49Cneo/R49Cneo αA-crystallin knock-in mice (3 months old) had a nearly complete cataract (stage 3–4). (D) R49Cneo/R49Cneo αA-crystallin knock-in mouse lenses showed a complete cataract at 5 months (stage 4). (E, F) Cataract in lens of a newborn R49C/R49C homozygous mouse with deletion of the neor gene by Cre-recombinase. Slit lamp image (E) shows a severe nuclear opacity at birth (stage 3). (F) Higher magnification of the lens shown in (E) shows the nuclear opacity covering ~70% of the lens.

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