Fig. S2

cdon^ATG MO efficiently interferes with cdon expression inducing morphants that present defects in the ventral region of the eye.

a) Schematic diagram of the strategy used to test the specificity of an antisense morpholino (MO) designed against the translation start site sequence of cdon (cdon^ATG). This MO or a standard control MO (MOct) were co-injected into medaka fish embryos with the cRNA of a reporter construct (5′cdon-GFP) carrying the zebrafish cdon 5′ sequence upstream of the gfp sequence. Translation of this construct (evident by expression of GFP) was efficiently knocked down by cdonATG MO (c) (25/25 embryos) but not by the MOct (b) (20/20 embryos). None of the two MO interfered with the translation of the GFP alone (d, e) (23/23 embryos). Bright field lateral (f-i) views of embryos injected with MOct (f, g) or cdonATG MO (h, i). cdonATG MO (h, i) but not MOct (f, g) injected embryos are characterized by alteration of the ventral retina (vr) at 28 hpf. The asterisks indicate the optic fissure in cdonATG morphant (i), which remains open at 36 hpf (compare insets in g, i). l, lens; vr, ventral retina. Scale bars: 40 μm (b-e). Scale bars: 100 μm (f-i).