Fig. 6

Fig. 6 Overexpression of slit2 at the late gastrula stage suppressed the convergent extension of the mesoderm. (A) The transgenic embryos (green) overexpressing the Slit2/GFP fusion protein and a wild-type sibling (dark) at 12 h which had been heat-shocked at 100% epiboly (10 h). (B, C) The slit2-overexpressing transgenic embryo which had been heat shocked at 80% epiboly suffered from severe cyclopia at 28 h. Frontal views of the wild-type sibling (B) and the slit2-overexpressing transgenic embryo (C). (D–I) Heat-shock induction of Slit2 at 80% epiboly impaired the convergent extension movement of the mesoderm and the anterior migration of the diencephalic cells. dorsal views, anterior to the top. The positions of the axial cells were examined by comparing the expression of axial mesoderm markers, hlx1 (D, G) and ntl (E, H), and the ventral forebrain marker, fkh5 (F, I), relative to the marker for anterior neural plate margin, dlx3 (D–I). Compared to the wild-type siblings (D–F), the transgenic embryos (G–I) overexpressing Slit2 by heat shock at 80% epiboly showed impaired convergent extension of the mesoderm and defect in the anterior migration of the diencephalic cells. (J, K) Normal embryos at 80% epiboly for comparisons. (L, M) Close-up views of the notochord of the normal embryo shown in E and the heat-shocked transgenic embryo shown in H, respectively. Bars, 250 μm (A, B–K), 50 μm (L and M).