Fig. 8. Depletion of β-catenin restores brain defects caused by MAK (hunk) MO. Embryos were injected with MAK MO (50 ng) and COMO (8 ng, A,C) or β-catenin MO (8 ng, B,D) into one dorsal animal blastomere at the four- to eight-cell stage. Whole-mount in situ hybridization of stage 19 embryos demonstrates that the effects of MAK MO on Otx2 and Gbx2 expression were partially reversed byβ -catenin MO (see also Table 2). Arrowheads in A and C indicate altered marker expression in MAK-depleted embryos. Nuclear βgal RNA served as a lineage tracer.
Image published in: Kibardin A et al. (2006)
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