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Fig. 2 Loss of Apc function leads to mispatterning of the retina. (A, B) Transverse toluidine blue stained sections of wild-type (A) and apc mutant (B) eyes. apc Retina is abnormal, with ectopic retinal pigment around the ONH (arrow). Ventral to the left. (C, D) Expression of irx1a, a marker for RGCs, is expanded in apc mutants (arrow in D). (E, F) Lateral view of wild-type (E) and mutant (F) eye labeled with α-zn8 antibody. Dashed line indicates eye outline as observed by DAPI. The RGC layer in apc mutants (F) is irregular and disorganized. (G, H) Snapshots of a 3D reconstruction of wild-type (G) and apc (H) GCL as observed using zn8 immunolabeling. The eye is displayed at frontal view in the first frame and is rotated by 45° in each consecutive frame. apc Mutant RGC layer is disorganized, with asymmetric distribution of RGC around the lens and RGCs that are not contained within the RGC layer (H). At the choroid fissure (arrow), RGCs are lacking. Widest diameter of RGC layer is 170 μm. (I–K) The mutant ONH and eyes are significantly smaller as determined by measuring ONH area (I) and the ratio of ONH size to eye size ( J; Student’s t-test p<0.01). (K) The percentage of the area covered by RGCs relative to the entire eye area shows that in apc mutants, there is a significant increase in the GCL area size as compared to wild types ( p<0.05). (C–H) Lateral view, anterior to the left. Apc, adenomatous polyposis coli; le, lens; ONH, optic nerve head. Error bars represent standard error of the mean (SEM). Scale bar = 50 μm.