Fig. 1.

fh20^-/- mutant embryos exhibit multiple defects including failure of facial branchiomotor neuron migration. Anterior is to the left in all panels. (B) The morphological phenotype of fh20^-/- embryos includes developmental delay and failure of tail elongation, absence of pigment formation, failure of the ventral retina to close, heart tube hypotrophy accompanied by pericardial edema, and degeneration of somites. The mutation is lethal at about 4 dpf. TUNEL labeling indicates that apoptotic cell death is increased in (D) fh20^-/- compared to (C) wild-type. (F) Facial branchiomotor neurons (asterisks) fail to migrate posteriorly from r4 in isl1-GFP transgenic fh20^-/- embryos compared to (E) wild-type. (G) Full-length wild-type spt5 mRNA injected into fh20^-/-embryos rescues facial branchiomotor neuron migration. (H) PCR genotypes for an absolutely linked microsatellite marker (30020R9) in (1) homozygous wild-type, (2) fh20^+/-, (3) fh20^-/-, and (4) the rescued fh20^-/- embryo shown in (G). In situ hybridization for ngn1 expression indicates a decrease in intensity that correlates with the fh20 mutation; (I) wild-type, (J) fh20^-/-. (K-L) Facial branchiomotor neurons, identified by islet1 in situ hybridization, migrate normally in the m806 point mutant of foggy/spt5 that abolishes the negative effect on transcript elongation. Scalebars = 900 μm (A, B) and 100 μm (C-L).