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Fig. 5. Antisense morpholino oligonucleotide MO1 does not affect the activin signal transduction pathway (A-F). Exogenous activin B can `rescue' the effects of MO1 (G-J). (A-F) Animal pole regions derived from uninjected Xenopus embryos or from those injected with MO1 (40 ng) form spheres (A,D), while those treated with activin (16 U ml–1) elongate (B). Elongation is substantially inhibited in animal caps derived from embryos injected with RNA (500 pg) encoding Xenopus follistatin (C) but not by 40 ng mMO1 (E) or MO1 (F). (G-H) Thirty-six percent of embryos injected into one cell at the four-cell stage with 2 pg RNA encoding mutated activin B-HA suffer defects in early development (H; compare with normal embryos in G), while 64% of embryos injected with 20 ng MO1 display a `knockdown' phenotype (I). Co-injection of mutated activin B-HA and MO1 `rescues' development, such that only 24% are abnormal (J).





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