Fig. 2

A loss of function mutation in zebrafish ns indicates redundancy between Gnl2 and NS. (A–D) The earliest visible defects that emerge around 24 hpf (A and B) in ns mutants (B) are the reduced forebrain (arrow), reduced eye size, thinner mid/hindbrain boundary (dashed line and arrowhead) and hyperinflated hindbrain ventricle. At 48 hpf, ns mutants (D) are characterized by smaller eyes, thinner mid/hindbrain boundary (dashed line and arrowhead) and severe hyperinflation of the hindbrain ventricle. (E) Schematic drawing of the NS protein with the position of the ns^hu3259 mutation indicated by the red dashed line. (F and G) gnl2 transcript is expressed throughout the brain at 30 hpf (F), with higher expression levels in the dorsal diencephalon, optic tectum, hindbrain and retina (inset in F). At 48 hpf (G), gnl2 transcript is expressed in the proliferative areas of the brain, namely the dorsal diencephalon, posterior optic tectum and hindbrain. In the retina, gnl2 expression is restricted to the proliferative ciliary marginal zone at 48 hpf (inset in G). ns transcript is expressed throughout the brain at 30 hpf (H), with higher expression levels in the dorsal diencephalon, optic tectum, hindbrain and retina (inset in H). At 48 hpf, ns transcripts are expressed in the dorsal diencephalon, posterior optic tectum and hindbrain (I). In the retina, ns is expressed in the ciliary marginal zone (inset in I). (J–M) The morphology of WT (J), single ns (K), single gnl2 (L) and gnl2/ns compound mutants (M) shows synergistic worsening of the mutant phenotypes, such as reduction of the telencephalon (arrows) and eye size, upon combined depletion of gnl2 and ns. All images are lateral view, with anterior to the left and dorsal up. d, dorsal diencephalon; e, eye; h, hindbrain; hv, hindbrain ventricle; ot, optic tectum. Scalebar 125 μm.