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. 2021 Jan 26;12(2):170. doi: 10.3390/genes12020170

Figure 4.

Figure 4

Foxc1a mRNA overexpression causes cardiac situs defects in a dose-dependent manner: (A–C) myl7 in situ hybridization of 75 pg foxc1a mRNA-injected embryos at 48 hpf, with representative images of the three cardiac looping morphologies provided (v, ventricle; a, atrium); (D) quantification of cardiac situs in control and foxc1a mRNA-injected embryos revealing an increasing prevalence of anomalous cardiac looping with increasing amounts of foxc1a mRNA; and (E) quantification of embryo situs defects in embryos injected with 75 pg of foxc1a mRNA. Statistical significance was apparent in comparisons between foxc1a/b and mCherry controls (cardiac: p = 0.0002 and 0.0012; gut: p < 0.0001 and 0.0205. mCherry vs. foxc1a and foxc1b respectively. One-way ANOVA and Dunnett’s post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).