Fig. 7. Slit1 can rescue the axonal phenotype caused by RCAS-Irx4 infection. Slit1 expression construct was co-electroporated with the RCAS-Irx4 construct. As the RCAS-Irx4-transfected cells would produce infectious viral particles that spread inside the retina, the infected area was larger than the Slit1-transfected area. Note in the area where a large number of Slit1-transfected cells were present (R in B; arrowheads in A,B), axonal phenotypes caused by RCAS-Irx4 infection were largely corrected. However, in the area that did not have Slit1-transfected cells (marked with NR in B), the axons were unevenly distributed and excessively fasciculated. (C) In the area where only a small number of Slit1-transfected cells were present, axonal phenotype was partially corrected. Interestingly, most of the transfected cells appear to align accurately with the axon bundles (arrowheads in C). The area shown in A-C was completely infected by RCAS-Irx4, confirmed by anti-GAG staining (D and data not shown). (E,F) As a control, an expression construct encoding GFP was co-electroporated with the RCAS-Irx4 construct. Although a large number of GFP-transfected cells were present in this area (visible over the staining of anti-GAG antibody, arrowheads in F), GFP could not rescue the axonal phenotype of RCAS-Irx4 infection and the axons appeared uneven and excessively fasciculated (E). The broken white arrows in A-C,E indicate the direction of axon projection toward the optic disc. Scale bar: 100 µm.

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