CPEB1 loss-of-function does not cause obvious retinal axon guidance defects. (A) Anti-green fluorescent protein (GFP) western blot on lysates of stage 24 embryos injected with 1 ng CPEB1-RBM-GFP mRNA with or without CPEB1 morpholino (MO) at the two-cell stage. CPEB1 MO effectively knocks down expression of CPEB1-GFP. (B) DiI filling of the retinal projection of stage 41 Xenopus embryos injected with CPEB1 MO at the two-cell stage shows no obvious defect in in vivo axon pathfinding. Uninj, uninjected. (C-G) Blastomere injection (C-D) and electroporation (EP) (E-G) of CPEB1 MO does not affect Sema3A-induced growth cone collapse. Blastomere injection (C) and electroporation (E, F) of carboxyfluorescein-tagged CPEB1 MO labels cell bodies (E) and growth cones (C, G) containing the MO with green fluorescence. (H) Beta-tubulin staining of wholemount mouse retinas shows no obvious defect in intraretinal guidance in embryonic day (E)18 CPEB1 knockout mice; retinal axons converge normally on the optic disc. (I, J) DiI filling of the retinal projection at E18–19 reveals no obvious defect in retinal axon guidance at the optic chiasm (F) or in the optic tract (G). Abbreviations: ch, optic chiasm; dLGN, dorsal lateral geniculate nucleus; sc, superior colliculus. Error bars represent standard error of the mean.