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Fig. 5. Shh inactivation affects differentiation and the development of late-born cell types. Retinal sections from wild-type (A,C,G,I,K,M,O) and {alpha}-Cre;Shh–/c mice (B,D,H,J,L,N,P) were stained at P0 for syntaxin (A,B) to identify amacrine and horizontal cells; at P6 for cone-arrestin (C,D) to identify cone photoreceptors; at P9 for Hoechst (G,H) to mark nuclei and for PKC (I,J) to identify rod bipolar cells; and at P6 for Hoechst (K,L), rhodopsin (M,N) to identify rod photoreceptor cells and CRALBP (O,P) to identify Müller glia. Red arrows in B indicate the line of differentiating horizontal cells in the outer plexiform layer in the periphery of the {alpha}-Cre;Shh–/c retina. Horizontal cells are not differentiated in the control retina at this stage (A). The intensity of cone arrestin staining is greater in the periphery of the {alpha}-Cre;Shh–/c retina compared with wild-type littermates (C,D). (E) Quantification of retinal cell types in the central and peripheral regions of the wild-type and mutant retinas at P1 (rods), P6 (cones, Müller glia) and P9 (bipolar cells). (F) The distribution of cells between the different retinal layers in a 100 µm region of the central and peripheral retinas of wild-type and mutant mice at P6. (G-J) Bipolar cells are reduced in number and disorganized in degenerating periperal retinas of {alpha}-Cre;Shh–/c mice. **P<0.05, *P<0.005. (K-P) Degenerative changes take place in the periphery of the {alpha}-Cre;Shh–/c retina, as indicated by the rosettes (arrows in L), gaps in rhodopsin staining (arrows in N) and infiltration of Müller glial cell bodies into the ONL (arrows in P). Scale bar: 100 µm.