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Pedigree and clinical manifestation of the left ventricular non-compaction (LVNC) in the affected members included in this study. (A) A pedigree of the family shows the number of affected members (affected members: shaded, WT: unshaded). A black arrow indicates the proband. Genotypes for the proband and all other family members are shown. (B) Echocardiograph (ECG) images of affected individuals with LVNC of the myocardium. (C) Magnetic resonance imaging (MRI) of thin epicardial and trabeculated endocardial layers of the ventricular wall.

Identification of the MYH7 heterozygous variant in the selected Iranian family. (A) Schematic diagram shows the human MYH7 locus and the enlarged sequences of exon 18 of this locus, along with the sequences of the MYH7 variation. The yellow region is the exon 18 sequences from MYH7. Green letters are wild-type DNA and the amino acid motif in the unaffected family members. Red letters indicate the substituted (C–A) target nucleotide in the MYH7 and the p.Leu655Met alleles in the affected family members. (B) Sequence chromatograms of the MYH7 novel variant loci which were found in this study. The results of Sanger sequencing from affected, unaffected, and control DNA samples confirmed that the variation was inherited from one of the parents in a heterozygous pattern. (C) Evolutionary conservation of MYH7 in the actin-binding site domain shows that this region of protein is highly conserved throughout all species, especially in Leu655.

Expression patterns of all MYH superfamily members during cardiac development. (A) Differential expression pattern of MYH7 in the mouse heart during 12 stages of development indicates that the expression of this gene plays an important role in the mouse cardiogenesis, especially during embryonic life. (B) Modeling scheme of the protein-protein interaction between native MYH7/actin and MYH7 p.Leu655Met/actin at the surface. Actin in the wild-type position is shown in green and in the mutant position, is shown in red. (C) Secondary structure cartoon representation. Actin in the wild-type position is shown in green, and in the mutant position, is shown in red. (D) The Leu655Met mutation is highlighted. Wild MYH7 protein (Leu 655) is shown in green, and the protein that has the mutated residue (Met 655) is shown in red.

The MYH7 deficiency causes cardiovascular defects in zebrafish. (A) Loss of MYH7 disrupts heart development. Lateral view of 3 and 5 dpf scramble gRNA injected control group and MYH7 KO larvae. Cardiac edema is clearly noticeable. Arrow at 3 dpf shows hemorrhage near heart. Edema accumulated around heart and spread to the abdominal area at 5 dpf. Arrow at 5 dpf shows enlarged heart. Scale bars: 200 μm in 3 and 5 dpf, 1 mm in middle 5 dpf. (B) The MYH7 knockout zebrafish has distorted cardiac chamber formation and looping as shown by fluorescence imaging of the Tg(actb2:hyper3) transgenic zebrafish reporter injected with scramble or MYH7 sgRNA. Representative images of control and mutant zebrafish are shown at 3, 4, and 5 dpf. Two different MYH7 KO fish at 3 dpf showed abnormal looping. Two different MYH7 KO fish at 4 dpf displayed enlarged and deformed ventricles. At 5 dpf, myh7 KO fish showed enlarged and granulated ventricle. Furthermore, a MYH7 mutant zebrafish with tubular heart is shown. Scale bars: 200 μm. (C)MYH7 is essential for proper formation of the cardiac ventricle and the pericardial cavity as shown by WMISH. Expression of MYH7, MYH7l, and mylk3 mRNAs is strongly reduced in MYH7 KO zebrafish at 4 dpf. MYH7 expression expands to the pericardial cavity and ventricular chamber in MYH7 KO fish at 5 dpf. MYH7l expression is reduced in MYH7 KO fish at 5 dpf. Expression of mylk3 in the cardiac ventricle of MYH7 KO larvae is disrupted at 5 dpf.