ZFIN Image: Venero Galanternik et al., 2015, Fig. S5

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Figure Caption

Fig. S5

Wnt/β-catenin upregulation in apcmcr mutants also leads to an Fgfdependent ectopic halo of pea3. Related to Figure 3 and Figure 6

(A-D′′) A 4-hour treatment of SU5402 inhibits Di-pERK1/2 in cells surrounding the primordium in sibling (A, C) and mutant embryos (B, D), demonstrating that ERK is Fgf dependent. (E-F) pea3 expression in siblings (E) and apcmcr mutant (F) embryos at 48 hpf. In apcmcr mutants the stalled primordium activates pea3 expression ectopically in cells surrounding the primordium. (G) Heat shock induced constitutive activation of Fgf signaling does not lead to ectopic filopodia formation in the lateral line. (H-K′) extl3/ext2 mutant embryos hyper-activate Di-pERK1/2 in primordium surrounding tissues like the skin compared to siblings. This phenotype is evident at 48 hpf (D-E′) and becomes more pronounced by 5 dpf (F-G′).

Acknowledgments

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