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. Author manuscript; available in PMC: 2019 Sep 19.
Published in final edited form as: Neuron. 2018 Sep 6;99(6):1145–1154.e6. doi: 10.1016/j.neuron.2018.08.019

Figure 2. Cadherins mediate interactions of V-ooDSGCs dendrites with an interneuronal scaffold.

Figure 2.

(A) V-ooDSGCs in control retinas, and retinas from which SACs had been killed by diphtheria toxin (ChATcre;CAGS-stop-DTR;Hb9GFP). Sections were co-stained for vesicular acetylcholine transporter (vAChT, red) to label SAC dendrites and neurotrace (NT, blue) to visualize somata. Stratification of VG3 amacrine cells, marked with anti-VGlut3 in separate sections, is unaffected. Scale bar, 20 μm.

(B) Mean GFP intensity (± SEM) of V-ooDSGC dendrites across the inner plexiform layer (IPL), derived from images such as those in A (n as in Fig. 1D). Lamination pattern of Cdh6-9-10 mutants is significantly different from that of controls (p<0.05; see Fig. 1 legend).

(C) Cdh6-9-10;Hb9-GFP alleles generated using CRISPR/Cas9-based genome engineering (see also Fig. S1K, L).

(D,F,H,J) V-ooDSGCs in control and mutant retinas at P21. Staining as in A.

(E,G,I,K) Mean GFP intensity (± SEM) of ooDSGC dendrites across the IPL, derived from images such as those in D,F,H,J, respectively. Lamination pattern of mutants differ significantly from those of controls (p<0.05 for E,G,I and p<0.01 for K; see Fig. 1 legend). n as in Fig. 1D. Bar in D is 20μm.

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