Fig. 1

Fig. 1

Mutations in glypican4 cause primordium migration defects. Anterior is to the left in all figures. (A) Lateral view of a 28 hpf wild type zebrafish embryo stained for glypican4 mRNA. (B) glypican4 in situ hybridization in a 32 hpf migrating primordium showing expression in the trailing region of the primordium and in the interneuromast cells (INM) deposited behind it. (C-D′) glypican4 is also expressed in muscle underlying the primordium all the way to the tail tip. (E) glypican4 is expressed in a deposited neuromast and (F) interneuromast cells at 32 hpf. (G-N) Embryos in the Tg(cldnb:lynGFP) background. The otic vesicle (OV) is used as a reference for primordium position along the embryo trunk. (G) Lateral view of a wild type 28 hpf embryo showing proper migration of the lateral line primordium. (H) Lateral view of a 28 hpf glypican4^fr6‘No-turning’ mutant. (I-L) About 40% of glypican4^fr6 mutant primordia possess a severe migration defect where the primordium makes a U-turn and migrates back toward the otic vesicle. This behavior occurs either very close to the otic vesicle without much migration toward the tail (I-J) or later when the primordium has already migrated partially along the tail (K-L). (M-N) Another less common phenotype observed in glypican4^fr6 mutants are primordia that shift their migratory path toward the pronephros. This phenotype can occur soon after migration has started (M) or when the primordium has already migrated a considerable distance (N). (O) Quantification of the observed glypican4^fr6 mutant phenotypes is represented in (H-N).