Patterns of gene expression in the PLL primordium. (A and B) Expression of cxcr4b and cxcr7b in 32-hpf control embryos. (C and D) Expression of cxcr4b in conditions of esr1 loss-of-function (C) and gain-of-function (D). The change in expression between A and C was observed in 75% of the injected embryos, respectively, the change between A and D in 30% of the injected embryos. (E and F) Expression of lef1 and cxcr7b in esr1 loss-of-function conditions. (G and H) Expression of cxcr7b (blue) and of gfp (brown) in a 32-hpf control cldnb:gfp embryo (G), in an sdf1-MO embryo (H; an extreme case of cxcr7b domain expansion is shown in I). (J–L) Rescue of cxcr7b expression in esr1-MO embryos that are also sdf1-MO (J), mutant for ody (K), or morphant for cxcr4b (L; note the nerve, arrowhead, extending from the ganglion, asterisk at the left of the figure, under the stalled primordium). (M and N) Expression of cxcr4b in 32-hpf sdf1-MO injected (M) or ody - (N) homozygous embryos; the photograph in N was taken under Nomarski optics to illustrate the extent of the primordium. (O and P) Expression of esr1 in a 32-hpf migrating primordium as revealed by fluorescent in situ hybridization using a rhodamine-coupled antidioxygenin antibody (O) and coexpression of esr1 and cldnb:gfp in the same embryo (P; confocal imaging). (A–F, K, and M) are bright-field pictures without Nomarski optics, to facilitate the detection of expression patterns. The primordia are outlined by dotted lines, based on images taken under Nomarski optics as illustrated in N. Double-headed arrows indicate the extent of the region where cxcr7b expression is not detectable.