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Fig. 2
Examples of PLL migration phenotypes observed in the screen. Phenotypes of 48hpf zebrafish embryos treated with small molecules that had been identified in the screen. (A) DMSO control. The red box indicates the successful migration of the terminal neuromasts to the end of the tail. Cldnb:EGFP embryos treated with 10µM of Se-(methyl)selenocysteine (C), Ellipticine (D) or 6(5H)-Phenanthridinone (E) show a delay in primordium migration and, therefore, have disrupted lateral line formation compared with the DMSO control (A,I), whereas treatment with Fenofibrate (B) or Kenpaullone (F) causes an increase in the neuromast deposition rate, resulting in a phenotype with premature deposition of terminal neuromasts. Treatments with the flavonoid-derivative molecules Purpurogallin-4-carboxylic acid (G) and 42-Methoxyflavone (H), almost completely abolished the posterior lateral line formation, generating PLL phenotypes of 1 (G) and 3 (H) deposited neuromasts, respectively. Arrows indicate the position of the PLLp relative to the fully successful migration marked by the red box in A; asterisks indicate the position of the last deposited neuromast in G and H. (I) Quantification of the average position of the final deposited neuromast in drug-treated embryos relative to the distance from the otic vesicle (ov) to the tip of the tail. Experiments were carried out using 15 larvae per condition. Error bars indicate +s.d. Compounds showed a variety of effects, from inhibiting both neuromast numbers and migratory behavior (e.g. Purpurogallin-4-carboxylic acid) to only slowing migration (Fenofibrate).