Loss of ATX-LPA1 signaling resulted in dyschondroplasia in zebrafish.

(a,b) Loss of ATX- LPA₁ signaling leads to deformation of the cephalic region in zebrafish embryos. Cephalic regions of wt and lpa₁ mutant zebrafish embryos (a) and cephalic regions of zebrafish embryos treated with LPA₁ antagonist, LPA₁ or ATX morpholinos (b) at 96 hpf (side view). Cartilage tissues visualized by alcian blue and alizarin red staining are also shown (ventral view). Scale bar: 100 µm. (c) Both lpa1 and atx are co-expressed with sox9, a marker of chondrocytes, in zebrafish embryo both at 72 and 96 hpf as judged by in situ hybridization. Scale bar: 50 µm. (d,e) Loss of ATX-LPA₁ signaling in zebrafish embryos leads to mislocalization of chondrocytes in cartilage tissues. (d) EGFP is expressed specifically in chondrocytes in col2:egfp transgenic zebrafish at 120 hpf. Scale bar: 100 µm. (e) In zebrafish embryos treated with LPA₁ or ATX morpholinos, chondrocytes are unevenly distributed in Meckel’s and ceratohyal cartilages at 120 hpf. Scale bar: 100 µm.

Loss of ATX-LPA₁ signaling resulted in dyschondroplasia in zebrafish.

(a) DNA sequence of wt and lpa₁ mutant zebrafish induced by tilling assay. The gene structure of zebrafish lpa₁ from exon1 –3 is also shown. (b) Cartilages of zebrafish embryo around 96 hpf visualized by alcian blue and alizarin red staining (dorsal view). Schematic diagram is also shown. (c,d) Loss of LPA₁ signaling leads to deformation of gill cartilages. Length of Meckel’s and ceratohyal cartilages in wt and lpa₁ mutant zebrafish (c) and in vehicle-or Ki16425-treated wt zebrafish (d) (Data are mean ± s.d., n = 20-22, **P<0.01, ***P<0.001). (e, f) Loss of ATX-LPA₁ signaling leads to deformation of cephalic region. Percentage of LPA₁ or ATX morphant embryos (e) and Ki16425-treated wt zebrafish embryos (f) with obvious cephalic malformation (Fig. 1b) is shown. (g) The expression patterns of slug and sox10, markers of CNCCs, in wt, LPA₁ or ATX morphant embryos. Scale bar: 50 µm.

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