Fig. 11
Fgf signaling is required for neuromast differentiation.
Control or Tg(sox10:DNerbb4) siblings were treated with DMSO or PD173074 at 32 hpf then fixed at 48 hpf. To verify that Fgf signaling was blocked, we performed in situ hybridazation for the Fgf target pea3 (A–D). (A) In controls treated with DMSO, pea3 is not expressed in interneuromast cells but is expressed in neuromasts (inset). (B) Control siblings treated with PD173074 show downregulation of pea3 in neuromasts (inset). (C) As shown for nrg1-3z26, Tg(sox10:DNerbb4) have an upregulation of pea3 within interneuromast cells. (D) This upregulation of pea3 is blocked by PD173074, illustrating that Fgfr signaling is inhibited. (E) In controls, atoh1a is only expressed in neuromasts (inset). (F) PD173074 decreases atoh1a in primary neuromasts (inset). (G) atoh1a is upregulated in differentiating interneuromast cells in Tg(sox10:DNerbb4). (H) This upregulation of atoh1a in interneuromast cells is completely blocked by PD173074, while some expression is still retained in primary neuromasts (inset).