ZFIN Image: Paone et al., 2018, Fig. 3

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Fig. 3

Smyd1a is required for proper sarcomere organization and can compensate for the loss of Smyd1b. (A) Co-immunostaining of plasmid (unc45b^min:smyd1b_tv1-gfp- or with unc45b^min:smyd1a-gfp) injected fla mutants with sarcomeric α-Actinin. [Scale bar: 20 μm]. (B) Flatline embryos were injected with either KCl (control), smyd1b_tv1 or smyd1a mRNA. At 72 hpf flatline mutants were identified and evaluated in regard to restored cardiac contractility. Shown are the mean percentages (+/− SD) of rescued fla embryos (n = 80) of four independent experiments. Statistical analysis was performed using one-way ANOVA (****p < .0001). (C) Measurement and statistical analysis as in (B) of ventricular FS of rescued fla mutants by injection of smyd1a- or smyd1b-mRNA at 72 hpf. Data are mean values ± SD. (D) Smyd1a specific ISH in fla mutants compared to control siblings (sib). (E) qRT-PCR analysis of smyd1a expression in control versus fla embryos.

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Acknowledgments

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