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Fig. 6

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ZDB-IMAGE-070917-51
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Figures for Pollard et al., 2006
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Fig. 6 Morpholino antisense knockdown of laminin α4 in bal mutants reveals redundant roles in notochord differentiation. Lateral views of 48 hpf control MO-injected embryos from a heterozygous bal cross showing a morphologically WT (A) and a bal mutant (B) (arrowhead; non-differentiated anterior notochord) embryo. From the same heterozygous bal cross, lama4 MO-injected embryos are also shown, ∼75% of embryos show a brain defect but no obvious notochord phenotype (C), whereas ∼25% of embryos have a severe notochord defect (D), with the entire anterior–posterior extent of the notochord disrupted. Whole mount laminin 1 antibody staining at 24 hpf shows expression of immunoreactivity in morphologically WT (E) and bal (F) mutant control MO-injected embryos. While ∼75% of lama4 MO-injected embryos have wild-type laminin 1 immunoreactivity (I), ∼25% (bal mutants) show severe loss of laminin 1 (J) (two independent experiments, total n = 136). Staining for expression of echidna hedgehog (ehh) at 24 hpf reveals the status of notochord differentiation in control MO-injected wild-type (G) and bal (H) mutant embryos. While lama4 MO-injected WT (K) embryos normally extinguish ehh expression, lama4 MO-injected bal mutant (L) embryos persistently express ehh.

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Reprinted from Developmental Biology, 289(1), Pollard, S.M., Parsons, M.J., Kamei, M., Kettleborough, R.N., Thomas, K.A., Pham, V.N., Bae, M.K., Scott, A., Weinstein, B.M., and Stemple, D.L., Essential and overlapping roles for laminin alpha chains in notochord and blood vessel formation, 64-76, Copyright (2006) with permission from Elsevier. Full text @ Dev. Biol.