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Fig. 1. Inhibition of XNF-ATc3 affects neural tube closure. (A) Embryos were either injected in the prospective ectoderm at the one-cell stage with 2 ng DN XNF-ATc3 or treated with 4 mM cyclosporin A (CsA) at stage 10 for 1 hour. Both sets were analyzed for Eng, Krox20, Six1, Pax3, Sox2 and HoxB9 expression at late neurula stages (19-21) by in situ hybridization. Neural tube closure defects were seen at concentrations as low as 250 pg DN XNF-ATc3. White arrowheads indicate expansions in the neural marker expression. (B) WT XNF-ATc3 rescues neural CE defects caused by CsA treatment. The graph represents three different experiments (n=731), which were normalized by the percentage of neural CE defects in embryos that were incubated in 400 μM CsA starting at the 64-cell stage. Co-injection of 2 ng WT XNF-ATc3(4) lead to a rescue of neural CE defects. |
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Fig. 3. Activation of XNF-ATc3 generates neural CE defects and anterior truncations. (A) Xenopus embryos were injected at the one-cell stage with 100 pg (middle panels) or 500 pg (right panels) of CA XNF-ATc3. Embryos injected with 100 pg CA XNF-ATc3 resembled control embryos during gastrula stages (first row, vegetal view of stage 11; second row, vegetal view of stage 12.5), but developed neural tube CE defects in 31% of embryos at neurula stages (third row: dorsal view of stage 17). Embryos injected with 500 pg CA XNF-ATc3 exhibited slight defects at stage 12.5 and neural CE defects in 81% of injected embryos. Control embryos developed no neural CE defects. (B) Xenopus embryos were injected at the one-cell stage with 50 pg CA XNF-ATc3 and analyzed for Krox20, Eng, Pax3, Sox2 and HoxB9 expression at the neurula stage. For XAG-1 in situ hybridization embryos were injected with 250 pg CA XNF-ATc3 and 100 pg lacZ (red) for lineage tracing. |
