Fgfr, Ras and MAPK synergize during formation of the posterior lateral line. Activity of Fgfr, Ras or MAPKK was modulated in claudinB:EGFP transgenic embryos using pharmacological inhibitors (SU5402 for Fgfr and PD0325901 for MAPKK) or expression of a dominant-negative transgene hsp70:dn-Ras between 30 and 48 hpf. (A) In 48-hour-old DMSO-treated controls, embryos have deposited 5-6 neuromasts (NMs) along the trunk, and the pLLp has reached the end of the tail to form the terminal cluster of neuromasts. (B) Treatment with an optimal dose of PD0325901 (7 μM) caused a failure of distal neuromast deposition and a stalling of the pLLp. (C) A suboptimal dose of MAPKK inhibitor PD0325901 (0.5 μM) did not affect neuromast deposition or pLLp migration. (D,E) Suboptimal inhibition of Ras (36°C heat shock of hsp70:dn-Ras transgenics) or Fgfr (treatment with 20 µM SU5402) did not affect neuromast deposition or pLLp migration. (F,G) Combining suboptimal PD0325901 treatment with suboptimal SU5402 treatment or suboptimal heat shock of hsp70:dn-Ras resulted in stalling of the pLLp and failed neuromast deposition. Scale bar: 200 μm.
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