Fig. 4

Increase in Wnt/β-catenin, Notch and Fgf signaling pathway gene expression in nrg1-3z26 mutant interneuromast cells.

Control siblings and nrg1-3^z26 mutants were processed for in situ hybridization at 48 hpf. A Wnt ligand, wnt10a, is not expressed in control interneuromast cells (A) but is increased in nrg1-3^z26 (B). The Wnt/β-catenin target gene lef1 is expressed in interneuromast cells in control siblings (C) but is greatly increased in nrg1-3^z26 (D). An additional Wnt/β-catenin target myca shows no expression in interneuromast cells (E) but strong expression in clumps of interneuromast cells in nrg1-3^z26 (F). ctnnb2 shows weak expression in control interneuromast cells (G) which is upregulated in nrg1-3^z26 (H). (I) In controls, notch3 is expressed in primary neuromasts (arrow) but not interneuromast cells. (J) notch3 is upregulated in mutant interneuromast cells. (K) In controls, the Notch target her4.1 is expressed in primary neuromasts (arrow) but not interneuromast cells. (L) In mutants, her4.1 is expressed in primary neuromasts (arrow) but is also increased in discrete clusters of cells (arrowhead). In controls the Fgf pathway genes including the receptor fgfr1a (M), the two ligands fgf3 (O) and fgf10 (Q) and the Fgf target gene pea3 (S) are all expressed in primary neuromasts (arrow) but not in interneuromast cells. All Fgf pathway genes, fgfr1a (N), fgf3 (P) fgf10 (R) and pea3 (T), retain expression in primary neuromasts (arrow) but are upregulated in interneuromast cells of nrg1-3^z26.