Alteration of N-CoR expression resulting in changes in r1–r6 hindbrain length that are similar to those caused by altering RA signaling in zebrafish embryos at 20 hpf. Embryos at 1- to 2-cell stages are microinjected with n-cor mRNA (C and D) or n-cor MO (I and J) to enhance or impair zebrafish N-CoR function, respectively. Alterations of RA signaling in embryos are performed by exogenous administration of 1 μM DEAB (E and F) or 10 nM RA (K and L) to reduce or enhance RA signaling, respectively. All treated embryos (C–F and I–L) together with wild-type control embryos (A and B) and control MO microinjected embryos (G and H) are grown to 20 hpf (22-somite stage) and then hybridized by RNA probes of engrailed2a (marking MHB), krox20 (marking r3 and r5) and hoxb4a (marking anterior boundary of r7). Whole mounted embryos (A, C, E, G, I and K) are positioned anterior left and viewed laterally whereas flat-mounted embryos (B, D, F, H, J and L) are positioned anterior left and viewed dorsally. The r1–r2, r3–r5 and r1–r6 lengths of the embryos overexpressing N-CoR (D) or treated with DEAB (F) are longer than those of the control embryos (B), respectively. The control MO microinjected embryos (H) have similar lengths of r1–r2, r3–r5 and r1–r6 to the control embryos (B). The lengths of r1–r2, r3–r5 and r1–r6 in the n-cor knocked down (J) or RA treated embryos (L) are shorter than those in the control embryos (B and H). MHB, midbrain–hindbrain boundary; r, rhombmere.
|
