Fig. 2

Knocking down n-cor resulting in elevation of endogenous RA signaling. Embryos at 1- to 2-cell stages are microinjected with n-cor MO (C and H) to knock-down n-cor expression or with dnN-CoR mRNA to reduce the function of N-CoR (E and J) and treated with 10 nM RA (D and I) to increase RA signaling. All treated embryos (C–E and H–J) together with wild-type control embryos (A and F) and control MO microinjected embryos (B and G) are grown to 20 hpf and examined for the expression of cyp26a1 (A–E) and aldh1a2 (also known as raldh2) (F–J), respectively, by whole mount in situ hybridization. All embryos are positioned anterior left and viewed laterally. cyp26a1 is mainly expressed at anterior epidermis, dorsal anterior spinal cord, somites and tail buds (A), while aldh1a2 is expressed at retina, branchial arches and somites (F) in the wild-type control embryo. Embryos microinjected with control MO display similar expression levels of cyp26a1 (B) and aldh1a2 (G) to the control embryos (A and F). Knocking down n-cor causes up-regulated expression of cyp26a1 in anterior epidermis and tail bud (C) and down-regulated expression of aldh1a2 in the regions of retina, branchial arches and somites (H). The expression changes also occur in the embryos treated with 10 nM RA (D and I) except that a strongly up-regulated expression of cyp26a1 in dorsal anterior spinal cord and somites in RA treated embryos (D). Overexpression of dnN-CoR causes up-regulated expression of cyp26a1 in dorsal anterior spinal cord and somites (E) and down-regulated expression of aldh1a2 in the regions of retina, branchial arches and somites (J). ae, anterior epidermis; as, anterior somites; ba, branchial arches; re, retina; s, somites; sc, dorsal anterior spinal cord; tb, tail bud.