Fig. 5. Morpholino generated loss-of-function phenotypes are rescued by ectopic protein. (A-D) Rescue of MOb1a phenotype, disposition of BM neurons is revealed with islet1: (A,B) islet-GFP transgenics; (C,D) islet1 in situ hybridization at 28 hours, anterior towards the left. (A,C) Embryos injected with MOb1a alone at 1 mg/ml, note lack of migration of r4-derived BM neurons (VII). (B,D) Embryos co-injected with MOb1a at 1 mg/ml and hoxb1a mRNA at 15 µg/ml, note rescue of migration of r4-derived neurons (VII), plus posteriorizing transformation of r2-derived neurons (VII’). (E-H) Rescue of MOb1b phenotype, embryos at 20 hours, anterior towards the top, krox20 in situ hybridization. (E) Uninjected wild-type control, note approximately equal AP extents of r3, r4 and r5; r4 size indicated with double-headed arrow. (F) hoxb1b mRNA injected (20 µg/ml) embryo, note no change in r4 size but increase in r3 AP extent, as we have previously described for gain-of-function experiments (McClintock et al., 2001). (G) MOb1b injected (4 mg/ml) embryo, note shift in r3/4 boundary towards the posterior, resulting in a significant reduction in AP extent of r4, together with increase in AP extent of r3. (H) Embryo co-injected with hoxb1b mRNA plus MOb1b, note rescue of r4 AP extent to wild-type proportions, together with increased size of r3 AP extent as seen with RNA alone.
