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. 2013 Apr 1;140(7):1457–1466. doi: 10.1242/dev.086850

Fig. 5.

Fig. 5.

Morpholino knockdown of JNK1 results in loss of cell-cell adhesion. (A,B,D,E) Embryos were injected with a control morpholino oligonucleotide (Cont MO; A,B,F,G,J,K,N,O) or a morpholino (MO) targeting Xenopus JNK1 (JNK1 MO; D,E,H,I,L,M,P,Q). (C) Knockdown of JNK1 protein and JNK activity (phosphoJun) is evident in extracts from JNK MO-injected (mosaic) guts, compared with Cont MO-injected gut extracts. (B,E) MOs were co-injected with mCherry mRNA as a lineage tracer to confirm gut targeted injection (red). (F-Q) Sections of Cont or JNK MO-injected embryos reveal the localization of atypical protein kinase C and mCherry (aPKC, green; mCh, red; F-I), E-cadherin and laminin (Ecad, green; lam, red; J-M), and integrin-β1 (Int, green, to delineate cell outlines; N-Q) in the gut. Endoderm cells in stage 46 Cont MO-injected embryos (red cells in F-G) undergo normal intercalation and epithelial morphogenesis, as indicated by the single layer of columnar epithelial cells (N-O) with normal E-cadherin (J,K). By contrast, endoderm cells with MO-disrupted JNK1 function (red cells in H,I) do not radially intercalate or form a normal epithelium, as indicated by their irregular cell shapes (P,Q) and reduced levels of E-cadherin (L,M). Asterisks indicate an inner population of endoderm cells. (G,K,O,I,M,Q) Higher magnification images of boxed areas in F,J,N,H,L,P, respectively. Scale bars: 50 μm.