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. 2003 Dec 15;17(24):3023–3028. doi: 10.1101/gad.1153603

Figure 3.

Figure 3.

The MAPK phosphorylation mutant LM-Smad1 inhibits endogenous CNS formation and neural induction by FGF8 or IGF2 signals. (A-H) Neurula-stage embryos in dorsal view, uninjected (control) or injected four times into the animal pole with WT-Smad1, LM-Smad1, or DM-Smad1 mRNA. (I-L) FGF8-injected embryos in anterior view. (M-P) IGF2-injected embryos in lateral view. Embryos were injected at the 8-cell stage into a single animal blastomere together with nuclear lacZ mRNA as lineage tracer and stained for Sox2. Stippled lines mark the lacZ-positive injection sites. Note that LM-Smad1, but not WT-Smad1, blocks neural induction by FGF8 or IGF2 mRNA. (Q) RT-PCR analysis of stage 26 ectodermal explants from embryos injected at the 8-cell stage with the indicated mRNAs. WE, whole embryo; Co, uninjected animal cap explants used as controls. The amounts of injected mRNAs per blastomere were 250 pg Smad1, 4 pg Chd, 100 pg FGF8, 800 pg IGF2, and 200 pg nuclear lacZ. Endogenous neural marker expression was inhibited in: A, 0/72; B, 0/46; C, 58/58; D, 0/35; E, 0/44; F, 37/78; G, 67/68; H, 9/23 embryos. Ectopic Sox2 expression was inhibited in: J, 0/23; K, 0/34; L, 24/32; N, 0/69; O, 0/53; P, 91/109 embryos. In (Q) one whole embryo or 10 animal caps were used per lane, two independent experiments.