Fig. 2. Retinal dorsoventral patterning defects in Bmpr1a^-/fx;Bmpr1b^+/-;Cre mutant mice. Control littermates shown are representatives of the Bmpr1a^+/fx;Bmpr1b^+/+;Cre or Bmpr1a^+/fx;Bmpr1b^+/-;Cre genotypes. (A) The Bmpr1a^-/fx; Bmpr1b^+/-;Cre mutants show no overt morphological defects in the eye. (B-E) Hematoxylin and Eosin-stained sections (B), ß-TubulinIII antibody staining for retinal ganglion cells (C), anti-PKC for bipolar cells (D) and anti-Syntaxin for amacrine cells (E) reveal that the retinal lamination pattern and cell types are unaltered in the Bmpr1a^-/fx;Bmpr1b^+/-;Cre mutants (bottom) compared with control littermates (top). (F) Analyses of retinotectal axon projection in the superior colliculus of the midbrain in postnatal day 7 (P7) animals. Focal injection of DiI into the dorsal retina of the left eye reveals a single termination zone in a lateral-posterior region of the contralateral (right) superior colliculus in normal animals (top, arrowhead). By contrast, in the mutants, several ectopic termination zones are seen (bottom, arrows), in addition to a normal lateral-posterior spot (bottom, arrowhead). The axes in the right superior colliculus are indicated: A, anterior; L, lateral; M, medial; P, posterior. (G-J) Coronal sections of embryonic eyes with dorsal towards top. In the mutants, the expression of dorsal markers Efnb2 (G) and Tbx5 (I) is lost, while transcripts of Ephb2 (H) and Vax2 (J), which are normally ventrally enriched, are now expanded throughout the developing retina (H,J). gcl, ganglion cell layer; inl, inner nuclear layer; le, lens; nr, neuroretina; prl, photo receptor layer. Scale bar: 500 µm in A,G,H; 100 µm in I,J.