FIGURE

Fig. 6

ID

ZDB-FIG-240620-111

Publication

Dong et al., 2024 - Deficiency in Prader-Willi syndrome gene necdin leads to attenuated cardiac contractility

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Fig. 6

MYL12.1 deficiency in zebrafish led to cardiac dysfunction (A) The expression of MYL12.1 and MYL12.2 genes in zebrafish heart as analyzed by using whole-mount ISH. Red arrowheads indicate the location of the heart. (B) The CRISPR-Cas9 technique was used to generate MYL12.1 allele in zebrafish. A gRNA targeting the exon 2 of MYL12.1 gene was injected with Cas9 protein into zebrafish embryos, resulting in a 2-bp deletion. (C) ISH was employed to validate the knockout of MYL12.1 in zebrafish. (D) The distribution of different genotypes in the zebrafishes harvested at 48 h postfertilization embryos or in adulthood. (E) Representative M-mode images (upper: wild-type zebrafish; lower: myl12.1+/? zebrafish). Double-headed arrows mark ventricle systolic and diastolic internal diameters, respectively. (F?H) The heart rate (F), ejection fraction (G), and fraction shortening (H) of adult WT and MYL12.1+/? zebrafishes as analyzed with echocardiograms. Data are presented as means ± SEM; ?p < 0.05, unpaired t test.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Phenotype Detail

Acknowledgments

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