FIGURE

Figure 4

ID

ZDB-FIG-231030-120

Publication

Huttner et al., 2023 - Loss of Sec-1 Family Domain-Containing 1 (scfd1) Causes Severe Cardiac Defects and Endoplasmic Reticulum Stress in Zebrafish

Other Figures

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Figure 4

Homozygous scfd1^vcc44−/− mutants show cardiomyocyte ultrastructure defects at 3 dpf. (A) Representative low (upper panels) and high (lower panels) magnification electron micrographs of cross-sections of the thinnest part of the ventricular wall illustrating reduced wall thickness in scfd1 ^vcc44−/− mutants (black two-headed arrows). my: myocardial cell (yellow outline); e: endocardial cell (green outline); L: lumen. White arrow heads point to sarcomere z-discs. (B) Representative low (upper panels) and high (lower panels) magnification electron micrographs of cardiomyocyte myofibrils. White arrow heads point to sarcomere z-discs. m = mitochondrium. (C) Scatter graphs quantifying z-disc number (per 80 µm² region of interest (ROI); n = 8–10 ROIs per fish per genotype) and z-disc width (n = 116–129 measurements per fish per genotype) in wildtype (+/+) and scfd1^−/− mutant cardiomyocytes. Results analyzed using two-way ANOVA showing significant genotype effects. Significance if p < 0.05. Created with BioRender.com.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	scfd1^vcc44/vcc44
Observed In:	ventricular myocardium cardiac muscle cell ventricular myocardium sarcomere ventricular myocardium Z disc
Stage:	Protruding-mouth

Phenotype Detail

Acknowledgments

This image is the copyrighted work of the attributed author or publisher, and ZFIN has permission only to display this image to its users. Additional permissions should be obtained from the applicable author or publisher of the image. Full text @ J Cardiovasc Dev Dis