XB-IMG-81711
Xenbase Image ID: 81711
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FIG. 3. Intracellular expression of Anti-FGFR1 scFvs blocks FGFR1 function in frog embryos to cause posterior defects. mRNA encoding either the anti-FGFR1 scFvs A2, C3, A7, A23, DNFGFR1, the noninhibitory FGFR1 HAV anti-ALK3 scFv-D1, anti-Erb-B2 scFv-F5, or the anti-cytochrome B scFv were injected into two anterior cells (the so-called dorsal cells) of four-cell stage frog embryos. A: When embryos reached the tadpole stage they were scored morphologically for defects in posterior development characteristic of disrupting FGFR1 function. The data in this graph were compiled from three separate experiments and the number of injected embryos is indicated. B: Expression of the anti-FGFR1 scFv-A2 caused embryos to develop with significantly reduced trunks and tails identical to the phenotypes caused by DN-FGFR1. C: Coexpression of wild-type FGFR1 with anti-FGFR1 scFv-A2 rescues the posterior defects caused by anti-FGFR1 scFv-A2 alone. D: Embryos expressing anti-FGFR1 scFv-A2 or the DN-FGFR1 developed with reductions in embryonic muscle (indicated with the arrow) compared to the normal amounts of muscle present in controls. Muscle was detected using whole-mount immunocyto- chemistry and the muscle-specific antibody 12/101 (Kintner and Brockes, 1984). E: Expression of anti-FGFR1 scFv-A2 or the DN-FGFR1 disrupted xbra expression. The CD1 cells of 16-cell embryos were injected with mRNAs encoding anti-FGFR1 scFv-A2, DN-FGFR1, or anti-ALK3 scFv-D1. At Stage 10 the embryos were analyzed for xbra expression using whole-mount in situ hybridization. i: Uninjected controls. ii: Embryos expressing DN-FGFR1. iii: Embryos expressing Anti-FGFR1 scFv-A2. iv: Embryos expressing Anti-ALK3 scFv-D1. Anti-FGFR1 scFv-A2 and the DN-FGFR1 caused disrupted xbra expression (the region marked by the arrows) while anti-ALK3 scFv-D1 did not. Reproduced with permission of the Publisher, John Wiley & Sons.
Image published in: Abler LL and Sheets MD (2003) Copyright © 2003. Image reproduced with permission of the Publisher, John Wiley & Sons.
Image source: Published
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