FIGURE

Fig. 5

ID
ZDB-FIG-190909-11
Publication
Bailey et al., 2019 - NAD+ improves neuromuscular development in a zebrafish model of FKRP-associated dystroglycanopathy
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Fig. 5

Fkrp morphants exhibit NMJ defects and NAD+ and EmergenC treatment prior to muscle development improves NMJ development. (A–D4) Anterior left, dorsal top, side-mounted embryos at 72 hpf with labeled AChR and SV2. (Lettered panels) Merged channels of AChR and SV2. (1) Skeletonized images. (2) Magnification of SV2 channel. (3) Magnification of AChR channel. (4) Magnification of skeleton channel. (A–A4) Control embryo. (B–B4fkrpmorphant embryo exhibiting reduced distributed innervation within the myotome. (C–C4fkrp morphant embryo treated with NAD+ at 6 hpf shows increased NMJs. (D–D4fkrpmorphant embryo treated with EmergenC at 6 hpf also shows increased NMJs. (E) Length of skeletons. Skeleton length is reduced in fkrp morphants (n = 153 half-myotomes) compared to controls (n = 144 half-myotomes) but significantly increased in fkrpmorphants receiving NAD+ (n = 183 half-myotomes) or EmergenC (n = 127 half-myotomes) at 6 hpf. (F) Degree of branching within the myotome in control embryos (n = 141 half-myotomes), fkrp morphants (n = 147 half-myotomes), and fkrp morphants receiving NAD+ (n = 179 half-myotomes) or EmergenC (n = 126 half-myotomes) at 6 hpf. Scalebars are 50 μm. *p < 0.05, **p < 0.01, ***p < 0.001, ns non-significant

Expression Data

Expression Detail
Antibody Labeling
Phenotype Data
Fish:
Conditions:
Knockdown Reagent:
Observed In:
Stage: Shield

Phenotype Detail
Acknowledgments
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