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. Author manuscript; available in PMC: 2011 Apr 30.
Published in final edited form as: Circ Res. 2010 Mar 25;106(8):1342–1350. doi: 10.1161/CIRCRESAHA.109.213132

FIGURE 5. Sodium channel knockdown results in reduced numbers of differentiating cardiomyocytes.

FIGURE 5

A. By in situ hybridization, scn5Laa and scn5Lab morphant embryos at the 16 somite stage display markedly reduced expression of nkx2.5 and of the myocardial sarcomeric genes cmlc2 and vmhc compared to control embryos. Treatment groups are as labeled. The number of embryos displaying the phenotype/the total number of embryos assessed is indicated in the lower right corner of each panel. B. Deficiencies in cardiac differentiation are not due to developmental delay. Shown is an embryo injected with the AB_MO2 morpholino compared to an uninjected clutchmate. Despite dramatic differences in the size of the heart field and head, both embryos have equivalent numbers of somites. C. Confocal reconstructions of the developing heart cone in Tg(cmlc2:GFP) embryos at the 22-somite stage (embryo in top panel is shown for orientation). Scale bar = 50µm. Scn5Laa morphant heart cones (AA_MO1, n=4) have significantly fewer differentiating cardiomyocytes than the heart cones of wild type (WT, n=6) and control-injected (AA_MIS1, n=3) clutchmates. Results are mean ± s.e.m. *, P<0.01 versus wild-type and †, P<0.01 versus AA_MIS1-injected, ANOVA.