STX12 deficiency‐induced cardiac morphological changes in zebrafish and mice. a–c) Knockdown of Stx12 in zebrafish led to pericardial edema. The phenotypes of zebrafish were represented at 2 dpf after injection of morpholinos into zebrafish eggs to knock down STX12 expression. Scale bar, 100 µm. d) Quantification of pericardial area. The pericardial area of zebrafish significantly increased after Stx12 knockdown (control‐MO, n = 10, E414‐MO, n = 10, t‐test, p < 0.0001; ATG‐MO, n = 10, p < 0.0001). e,h) Cardiac stereomicroscopic images of P0 Stx12‐KO (e) and wild‐type littermates (h). Stx12‐KO heart exhibited cardiac malformation. Scale bar, 500 µm. f,g,i,j) Hematoxylin and eosin (HE) staining of coronal section (f, i) and cross section (g, j). Scale bars, 500 µm. k) Scatterplots with boxplots showed that heart weight‐to‐body weight ratio was significantly increased in Stx12‐KO mice (WT, n = 9, KO, n = 11, p = 0.0003). l,m) WGA staining of Stx12 myocardial‐specific knockout mice and Stx12‐flox control mice. Scale bar, 10 µm. n) Quantitative analysis of WGA staining (Flox‐control, n = 9, cKO, n = 9; p = 0.0272). o) Scatterplots with boxplots showed that the heart weight‐to‐body weight ratio was significantly increased in myocardial‐specific Stx12 knockout mice compared to Stx12‐flox control mice (Flox‐control, n = 10, cKO, n = 10, p = 0.0372). Statistical results: *p < 0.05, ***p < 0.001, ****p < 0.0001; t‐test.
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