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. 2012 Jul 4;32(27):9429–9437. doi: 10.1523/JNEUROSCI.0394-12.2012

Figure 1.

Figure 1.

An Otx2 motif necessary for binding to cortical sections. A, Putative GAG-binding motif (in red) in the Otx2 N-terminal region bears an RK doublet just before the homeodomain. RK and AA peptide sequences are indicated. B, Schematic representation of AP fusion proteins used in binding experiments: AP-NtHD contains amino-acids 1–98 including the RK doublet and homeodomain; AP-Nt(AA)HD, in which the RK doublet is mutated to an alanine doublet; and AP-HD composed of AP fused directly to the homeodomain (aa 38–98) without the RK doublet. Nonfused AP was used as a negative control. C, E, F, AP staining on fresh-frozen sections reveals AP-NtHD (C) but not AP (E) or AP-HD (F) binding to cells in the posterior cortex (V1). D, Full-length Otx2 disrupts AP-NtHD cortical binding (D). G, H, Higher magnification of V1 sections shows AP-NtHD binding (G) but not AP-Nt(AA)HD binding (H). I, J, RK (I), but not AA (J), peptide antagonizes AP-NtHD binding. K–N, ChABC treatment of frozen sections abolishes WFA staining (K, L) and prevents AP-NtHD binding (M, N). Scale bars: (in C) C–F, 350 μm; (in G) G–J, 100 μm; (in K) K, L, 100 μm.