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Fig. 1 β-Aminopropionitrile recapitulates the notochord phenotype of copper deficiency. Wild-type embryos were incubated in vehicle (A), 10 μM neocuproine (B), or 10 mM β-aminopropionitrile supplemented with 10 µM CuCl2 (C). At 48 hpf, the notochord (arrowheads) is distorted in embryos treated with neocuproine (B) and β-aminopropionitrile (C); however, melanocytes (arrows) are present after β-aminopropionitrile (C) but not neocuproine treatment (B), demonstrating that β-aminopropionitrile does not act through copper chelation.
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Reprinted from Developmental Biology, 307(2), Gansner, J.M., Mendelsohn, B.A., Hultman, K.A., Johnson, S.L., and Gitlin, J.D., Essential role of lysyl oxidases in notochord development, 202-213, Copyright (2007) with permission from Elsevier. Full text @ Dev. Biol.