Fig. 6. RGC axon guidance defects in ThyCreShh^n/c mice. (A,D) Hematoxylin and Eosin staining of sections through the optic disc of E12 wild-type (A) and ThyCreShh^n/c (D) embryos. Note that in the wild type, the eosinophilic RGC axons are separated from the potential subretinal space (black asterisk in A) by the optic disc astrocyte precursor cells (white arrows in A), and that these cells are missing in ThyCreShh^n/c mutants (D) thereby exposing the subretinal space (black asterisk in D) to invasion by RGC axons (white asterisk in D). Anti-neurofilament-associated protein immunostaining (B,C,E,F) of E17 retinal sections of wild-type (B) and ThyCreShh^n/c embryos (C,E,F) reveals the retinal axon guidance defects of ThyCreShh^n/c embryos. Compared with wild type (B), ThyCreShh^n/c embryos display axon coiling in the subretinal space at the optic disc (white asterisks in C and D), and axon misrouting into the peripheral retina (open white asterisks in E,F). Note the severe axon misguidance in (F) that creates what looks like multiple optic discs (white arrows in F).