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. Author manuscript; available in PMC: 2006 Apr 26.
Published in final edited form as: Exp Cell Res. 2005 Aug 15;308(2):364–380. doi: 10.1016/j.yexcr.2005.04.035

Fig. 6.

Fig. 6

DmVav induces defects in embryonic dorsal closure. To show defects in the ectoderm, embryos were stained with an anti-fasciclin III antibody followed by a FITC-labeled secondary antibody. (A) Expression of DmVav (Δ1–207) results in a failure in dorsal closure. The limit of the unclosed area in the 16-stage embryo is indicated with a discontinuous white circumference. (B) Ectoderm histology of wild type (panels A and C) and DmVav (Δ1–207)-expressing embryos (panels B and D) at stage 13. Note that the distribution of fasciclin III in the cells of the leading edge in experimental embryos (B, D) is abnormal, being detected in the dorsal side of these cells from where it is excluded in wild type embryos (A, C). The magnification used was 20× (for panels A and B) and 40× (for panels C and D).