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Fig. 3. Histological analysis of {alpha}A-Alk6DN and EE-1.0-K-Alk6DN transgenic lenses. E13.5 Hematoxylin and Eosin stained sections of wild-type mouse eyes (A), and homozygous mice of the {alpha}A-Alk6DN-11 (B) and EE-1.0-K-Alk6DN-48 (C) transgenic lines. The black arrowheads indicate the normal nasal side equatorial structure in wild-type mice (A) and the abnormal form (B,C) seen with both transgenic mouse constructs. (D-F) {gamma}-crystallin immunolabeling of E13.0 lenses from wild-type mice (D) and from homozygous {alpha}A-Alk6DN-11 (E) and EE-1.0-K-Alk6DN-48 (F) transgenics. The white arrowheads indicate the nasal side domain in which primary fiber cells have low {gamma}-crystallin levels. Similarly, MIP26 immunolabeling in wild-type E13.0 mouse lenses extends to the equator (G), while in homozygous {alpha}A-Alk6DN-11 (H) and EE-1.0-K-Alk6DN-48 (I) transgenics of the same age, there is a nasal side region in which labeling is absent or low. Sections in A-I are located in the ventral half of the lenses shown. (J-L) Day-of-birth Hematoxylin and Eosin stained sections of the eyes of wild-type mice (J), and homozygous mice of the {alpha}A-Alk6DN-11 (K) and EE-1.0-K-Alk6DN-48 (L) transgenic lines. This shows that the transgenic lenses are smaller and have emphasized suture spaces (J-L, arrowheads) owing to the lack of complete elongation of the primary fiber cells. (M-O) A comparison of whole-mount lenses dissected from wild-type (M) and homozygous {alpha}A-Alk6DN-11 (N) and EE-1.0-K-Alk6DN-48 (O) mice showing the refractile anomaly present in the transgenics (N,O, red arrowheads).





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