Fig 7

Fig 7

Representative confocal images of dorsal head periderm of control (A), myoVb MO (B), grhl3 MO (C), grhl3 MO;myoVb MO (D) at 48 hpf, stained with anti-E-cadherin antibody (red). Scale bar in D (for A-D) = 50 μm. Increased localization of E-cadherin in myoVb morphants is absent in grhl3;myoVb double morphants. Representative bright field images showing expression of cdh1 (E-cadherin) by WISH in the above four conditions (E-H). Note the increased patchy expression of cdh1 adjacent to regions having cell rounding in myoVb morphants, which is absent in grhl3;myoVb double morphants. Assessment of retention probability of Grhl3 deficient cells in MyoVb deficient periderm. Control (I) and grhl3 morphant clones (J) in myoVb morphant embryonic epidermis (I, J), control morphant clones (K,L) in grhl3 morphant (K) and grhl3;myoVb double morphant epidermis (L). Clones are marked with GFP (green). Anti-E-cadherin staining marks cell boundaries (red). Confocal images of peridermal clones overexpressing Cdh1-mCherry (red) in control (M), grhl3 morphant (N) and grhl3;MyoVb double morphant (O) epidermis. All cell boundaries are marked by anti-E-cadherin antibody (green). Scale bar in L, M = 50 μm. Graph representing proportion of embryos retaining the clones under given genetic conditions (P). % embryos showing peridermal clones per set are plotted as individual points, horizontal line denotes the median value. Note that grhl3 morphant clones are retained rarely in myoVb morphant epidermis. While clones retention is very low in grhl3;myoVb double morphant embryos, cdh1 overexpression partially rescues this phenotype. A schematic (Q) showing Grhl3 functioning in retention of rounded cells by strengthening E-cadherin mediated cell-cell adhesion.