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Fig. 1

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ZDB-IMAGE-161229-8
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Figures for Venero Galanternik M. et al., 2016
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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 glypican4fr6No-turning’ mutant. (I-L) About 40% of glypican4fr6 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 glypican4fr6 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 glypican4fr6 mutant phenotypes is represented in (H-N).

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Reprinted from Developmental Biology, 419(2), Venero Galanternik M., Lush, M.E., Piotrowski, T., Glypican4 Modulates Lateral Line Collective Cell Migration Non Cell-Autonomously, 321-335, Copyright (2016) with permission from Elsevier. Full text @ Dev. Biol.