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Fig. 5 | Journal of Animal Science and Biotechnology

Fig. 5

From: Sequential disruption of ALV host receptor genes reveals no sharing of receptors between ALV subgroups A, B, and J

Fig. 5

a Schematic representation showing the wild-type TVA receptor (WT TVA) and modified TVA receptor (TVA(+ 1), TVA(− 3) and TVA(∆1–6)) overexpression cassette and sequencing results of the constructed vector. CMV promoter and TVA CDS sequences are described, and modified nucleic acids are highlighted. 5′-TR: piggyBac 5′-terminal repeat; Neo: neomycin resistant gene; CMV: cytomegalovirus promoter; 3′-TR: piggyBac 3′-terminal repeat; Amp: ampicillin resistant gene; CAGG: cytomegalovirus (CMV) enhancer fused to the chicken beta-actin promoter; PBase: piggyBac transposase coding sequence. b Expression of GFP by virus-infected DF-1 clones. WT TVA or modified TVA receptors overexpessing WT DF-1 cell lines (WT, WT + TVA, WT + TVA(+ 1), WT + TVA(− 3) and WT + TVA(∆1–6)) and tva-modified DF-1 clones (3 bp deletion on tvb) (TVA#1–5, TVA#1–5 + TVA, TVA#1–5 + TVA (+ 1), TVA#1–5 + TVA(− 3) and TVA#1–5 + TVA(∆1–6)) were examined under a fluorescence microscope. Scale bar = 100 μm. c, d Flow cytometry analysis of virus-infected DF-1 clones. Gray peaks indicate the population of the DF-1 not infected with ALV subgroup A (negative control; WTni and TVA#1-5ni) and green peaks indicate the population of ALV subgroup A-infected DF-1 clones. The numbers on the histograms represent the mean percentage of cells within that population of triplicate replications. WT DF-1 fibroblasts were used as the control (positive control). d Data represent the mean ± SEM of triplicate replications. Different letters (a, b) indicate significant differences (P < 0.05)

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