Figure 7. Kdm2a/b Regulate β-Catenin in Xenopus Embryos and Gene Expression Involved in A-P Axis Formation (A and B) Knockdown of Kdm2a or Kdm2b led to incremental changes in non-phosphorylated β-catenin in gastrula embryos. Error bars represent SEM in triplicate. ∗p < 0.05; ∗∗p < 0.01. (C) Knockdown of Kdm2a or Kdm2b enhanced β-catenin methylation in gastrula embryos. (D) Simultaneous knockdown of Kdm2a and Kdm2b led to the synergistic enhancement of β-catenin methylation in gastrula embryos. (E) Knockdown of Kdm2a or Kdm2b upregulated the activity of the Wnt-responsive luciferase reporter in embryos. Error bars represent SEM of four replicates. ∗p < 0.05; ∗∗p < 0.01. (F and G) β-catenin knockdown rescued the developments defect (F) and the upregulation of gene expression (G) that were caused by double knockdown of Kdm2a and Kdm2b. In (F), all embryos are shown in lateral view with the anterior to the left. In (G), all embryos are shown in dorsal view with the animal pole to the top. (H) In embryos at st. 12, the increase in β-catenin after double knockdown of Kdm2a and Kdm2b was weakened by β-catenin knockdown. In (A)–(E), 30 ng of ctrlMO or Kdm2aMO and 20 ng of Kdm2bMO were injected individually. When injected together (D), the dose for each MO was reduced by half. In (F), 20 ng of ctrl MO, 10 ng of Kdm2aMO, 5 ng of Kdm2bMO, and 5 ng of β-CatMO were injected. In (G) and (H), 30 ng of ctrl MO, 15 ng of Kdm2aMO, 10 ng of Kdm2bMO, and 10 ng of β-CatMO were injected. WCLs of injected embryos were used for IB in (A), (C), (D), and (H).
Image published in: Lu L et al. (2015)
Copyright © 2015. Image reproduced with permission of the Publisher, Elsevier B. V.
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