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. 2016 Nov 1;143(21):3994–4002. doi: 10.1242/dev.137760

Fig. 1.

Fig. 1.

Loss of function of Lhx2 in neuroretina led to microphthalmia and lens development defects. (A,B) Lateral view of control (A) and Chx10-Cre;Lhx2lox/lox animals (B) indicating microphthalmia in Chx10-Cre;Lhx2lox/lox animals. (C-F) Hematoxylin and Eosin staining of eye sections from E13.5 (C,D) and P0.5 (E,F) of control (C,E) and Chx10-Cre;Lhx2lox/lox (D,F) mice. Dotted green and black outlines mark the retinas and lenses, respectively (C-F) and insets (D,F) are digital zooms of the boxed regions. (G) Graph indicating average neuroretinal area and lens area in sections of control and Chx10-Cre;Lhx2lox/lox mice at P0.5. Data were analyzed using unpaired two-tailed t-test; n=7 for Chx10-Cre;Lhx2lox/+; n=11 for Chx10-Cre;Lhx2lox/lox; ****P<0.0001. Scale bars: 5 mm in A,B; 100 µm in C-F.