Fig. 1. Morphology of spg mutants. (A-D) Lateral views. (E-H) Dorsal views. (A) Wild-type embryo at 26 hours post fertilization. c, cerebellum; h, hindbrain; o, otic placode; t, tectum. (B) spghi349 homozygous mutant embryo at 26 hpf. There is significant variability of the phenotype. The hindbrain displays disorganization (left arrowhead) and the otic placode is reduced in size, containing only one otolith (right arrowhead); note the proximity of the otolith to anterior brain structures when compared with wild type. (C) spge68 homozygous embryos are less affected at the hindbrain than the insertional mutant (B). (B,C) In spg mutant embryos, no proper MHB structures are visible (red and white arrowheads, respectively). (D) The spghi349 mutation causes a variable shortening and altered morphology of the tail. The embryo at the top is wild type, and the two beneath are both spghi349/spghi349. The effect varies from a very minor kink to major shortening and structural defects (see arrowheads). (E,F) -acetylated tubulin staining recognizing the axonal scaffold in the developing brain at 28 hpf. (E) Wild type. Six bilateral transverse axon bundles mark the borders between single rhombomeres. (F) spg mutant embryo shows strong disorganization of the axonal scaffold within the hindbrain. (G,H) Staining with the monoclonal antibody 3A10 at 30 hpf. (G) The Mauthner neurons in the wild-type embryo are marked with a red arrowhead. (H) spghi349/spghi349 mutant embryo showing complete absence of the Mauthner neurons.