Reduced responsiveness of gemin3, gemin5, and smn1 mutants to ErbB pathway inhibitor AG1478.a Neuromasts in AG1478-treated control and gemin5hg81 mutant embryos at 5 dpf. Neuromasts are shown as white dots. Scale bar, 250 µm. b Quantification of the lateral line neuromasts in mock and AG1478-treated embryos carrying the gemin5hg81 mutation at 5 dpf. c Quantification of the lateral line neuromasts in mock and AG1478-treated embryos carrying the smn1hg104 mutation at 5 dpf. d Quantification of the lateral line neuromasts in mock and AG1478-treated embryos carrying the gemin3hg105 mutation at 5 dpf. e Quantification of the lateral line neuromasts in mock and AG1478-treated embryos carrying the gemin6hg110 mutation at 5 dpf. Error bars in the graphs show the mean ± s.e.m. ns, P > 0.05; *P < 0.05; **P < 0.01; ****P < 0.0001. f Fluorescent images of lateral line neuromasts labeled by transgenes Tg(pou4f3:GAP-GFP) and Tg(SqET20:EGFP) in the control and gemin5hg81 mutant at 5 dpf after AG1478 treatment. Images were taken in the areas surrounding the end of yolk extension. White arrow points to the Tg(SqET20:EGFP) signal in the control embryo, which is dramatically increased in the mutant. Scale bar, 50 µm. The embryos used for the above analyses were generated from a pairwise incross of heterozygotic parents, treated with 2 µM AG1478 from 1 to 5 dpf, and then used Yopro-1 staining or transgenic fluorescence at 5 dpf to analyze neuromast formation. Data for each condition were generated using ~40 embryos born from a single pair of heterozygous parents.
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