|
Fig. 4 Components of JNK Signaling Are Required for Axin-Induced Dorsalization (A) Injection with 50 pg of axinΔMID mRNA caused embryonic ventralization only. The top panel on the left shows an illustration of axinΔMID structure. Live ventralized embryos at 24 hpf lack the head and the notochord, but possess an enlarged blood island (indicated by an arrow). The right panel shows that axinΔMID overexpression inhibited gsc and chd expression (dorsal views) but expanded bmp2 and drl expression (animal pole views with dorsal to the right) at the shield stage. (B) Statistical data for axinΔMID overexpression. Upward and downward arrows indicated increased and decreased expression, respectively. (C and D) MKK4 siRNA, MKK4-KM (C), and JNK-APF (D) abolish axin-mediated JNK activation. FLAG-tagged JNK was cotransfected with different constructs as indicated on the top. JNK activities from different transfections were determined as described in Figure 2. (E–H) Percentages of dorsalized and ventralized embryos, judged by morphological changes at 24 hpf (E and G) or by marker changes at the shield stage (F and H). Injection dosages: axin mRNA, 200 pg; MKK4-KM mRNA, 300 pg; JNK-APF mRNA, 300 pg.
Reprinted from Developmental Cell, 13(2), Rui, Y., Xu, Z., Xiong, B., Cao, Y., Lin, S., Zhang, M., Chan, S.C., Luo, W., Han, Y., Lu, Z., Ye, Z., Zhou, H.M., Han, J., Meng, A., and Lin, S.C., A beta-Catenin-Independent Dorsalization Pathway Activated by Axin/JNK Signaling and Antagonized by Aida, 268-282, Copyright (2007) with permission from Elsevier. Full text @ Dev. Cell