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Fig. 4. Rescue of the integrity of the LE. (A-C) Schematic representation of (A) full-length E-cadherin (ECad), (B) an ECad mutant protein that lacks the Arm binding domain encoded by the shg^g317 allele and (C) a fusion protein where ${alpha}$ -catenin is fused to the C-terminus of full-length ECad (ECadFL– ${alpha}$ -catenin). The ability of this chimera to recruit Arm (Hii) is schematized. (D) Cuticle of shg^g317 embryos showing a dorsal hole (see Table 1 for percentages of phenotypes). (E) Cuticle of a shg^g317 embryo expressing ECadFL– ${alpha}$ -catenin in the engrailed domain, showing a complete rescue of the dorsal hole characteristic of shg^g317 embryos. Mismatches can be observed (arrowhead). (F) Cuticle of a shg^g317 embryo expressing ECadFL– ${alpha}$ -catenin in the AS, showing a complete rescue of the dorsal hole. (G-J) embryos stained for actin (phalloidin-TxR), ECad (green) and Arm (white, shown as a separate channel in Hii and Iii). (G) shg^g317 embryo showing the loss of adhesion between AS and epidermis. (Hi) embryo of the same genotype as in E, showing the rescue of the adhesion between AS and epidermis. Note the elongation of DME cells. (Ii) Embryo of the same genotype as in F, showing that the expression of ECadFL– ${alpha}$ -catenin in the AS rescues the adhesion between the AS and the epidermis. (J) shg^g317 embryo expressing a wild-type form of ECad fused to GFP (UAS-ECadGFP) in the engrailed domain, showing local rescue of the adhesion between the AS and the epidermis.

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