Fig. 4. Intraretinal axonal phenotype caused by RCAS-Irx4 virus infection. Retina development is more advanced in the center than in the periphery. The axons in the wild-type E8 retina were stained with the anti-neurofilament antibody 270.7 (A,B). (A) At the periphery, axons join and leave fascicles, producing a `honeycomb' appearance. (B) Close to the center of the retina, the axons appear more mature and fasciculated. (C-H) Optic vesicles were infected with RCAS-Irx4 virus (E-H) or control RCAS-GFP (C,D) at HH stage 10-11 (E1.5) and the infected retinas were harvested at E8. Flat-mounts of retinas were double stained with a mouse monoclonal antibody recognizing neurofilament (270.7) (C,E,G) and a rabbit polyclonal antibody recognizing viral antigen (anti-p27) (D,F,H). Images in C,E and G are in the same fields as in D,F and H, respectively. The broken white arrows in A-C,E,G indicate the direction of axon projection toward the optic disc. (C,D) The axons in the control RCAS-GFP virus-injected retina appear normal. (E,F) Close to the infected/uninfected boundaries, some axons appear to turn slightly towards the uninfected area (arrowhead in E). (G,H) In the center of the infected area, an abrupt increase of fasciculation of the axon bundles was observed (arrowheads in G) when axons went from an uninfected (UI) to an infected (Ib) area. The axons returned to wild-type appearance when they went from infected (Ia) to uninfected (UI) area, suggesting that the changes in axonal morphology in the infected area were reversible. Scale bar: 100 µm.

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