wnt3a MOs can enhance dorsal-ventral (D/V)and anterior-posterior (A/P) patterning defects associated with mild loss of wnt8 function. Embryos were injected with 2 mg/ml wnt3a MO (B,F), 0.25 mg/ml each of wnt8 ORF1 and ORF2 MOs (C,G), or both (D,H). (A-D) Animal pole views, dorsal to the right. Embryos were fixed at 60% epiboly and stained with flh to visualize the dorsal organizer, the limits of which are demarcated by arrows. wnt3a MO injection has no effect on the size of the organizer (B). At these doses, wnt8 MOs result in only a slight expansion of the flh domain (C), while injection of both morpholinos results in a significant expansion of the dorsal organizer (D). (E-H) lateral views, dorsal to the right. Embryos were fixed at 100% epiboly and stained with opl, to mark the prospective telencephalon, pax2, to mark the future midbrain/hindbrain boundary, and tbx6, to mark the margin. Neither wnt3a MOs (F) nor wnt8 MOs (G) caused any defects in A/P patterning of the neurectoderm, but wnt3a/wnt8 morphants showed a dramatic expansion of opl (H), reflecting the increased anterior character of the neurectoderm. With the higher doses of wnt8 MOs used for the other experiments in this paper, co-injection of wnt3a MOs does not enhance D/V and A/P patterning defects.
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