FIGURE

Fig. 2

ID

ZDB-FIG-180608-89

Publication

Paone et al., 2018 - Loss of zebrafish Smyd1a interferes with myofibrillar integrity without triggering the misfolded myosin response

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Fig. 2

Knock-down of smyd1a leads to defective skeletal muscle and heart function. (A) Zebrafish embryos at 48 hpf injected either with an morpholino against smyd1a (MO1-smyd1a) or the respective control (Ctrl-MO1). (B) Quantification of ventricular FS in % (n = 6) from A and B at 72 hpf. Shown are mean values of three independent experiments with error bars representing standard deviation (SD). Statistical analysis was performed using one-way ANOVA followed by tukey's multiple comparison analysis (****p < .0001). (C) Quantification of the touch-evoke response assay. Smyd1a morphants were analyzed in regard to their adequate touch responsiveness upon mechanical stimulus. Shown are mean values (+/− SD) in percent of three independent experiments. Statistical analysis was performed as in (B) (C) Birefringence images of embryos (48 hpf) injected with Ctrl-MO1, MO1-smyd1a or Cas9 + smyd1a-gRNA ribonucleoprotein(RNP) complex. (E) Electron micrographs of skeletal muscle cells of smyd1a morphants versus control embryos at 48 hpf.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	WT + CRISPR2-smyd1a WT + MO4-smyd1a WT + MO5-smyd1a
Knockdown Reagents:	CRISPR2-smyd1a MO4-smyd1a MO5-smyd1a
Observed In:	pericardium skeletal muscle skeletal muscle myosin filament skeletal muscle cell sarcomere skeletal myofibril assembly thigmotaxis
Stage:	Long-pec

Phenotype Detail

Acknowledgments

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