Fig. 2

Fig. 2

Loss of Zfpm1 results in cardiac chamber maturation defects. (A) Representative images of dissected hearts from Zfpm1^-/- and WT sibling fish at 60 dpf. a, atrium; v, ventricle; oft, outflow tract. Scale bar: 200 µm. (B) Histological analysis of Zfpm1^-/- and WT sibling fish. Heart sections were Masson's trichrome stained. Scale bar: 100 µm. (C) Representative images of ventricle sections stained with WGA to indicate cardiomyocyte cell size at 60 dpf. Scale bar: 10 µm. (D) Transmission electron microscopy (TEM) on control and Zfpm1^-/- hearts revealed no overt defects on myocardium ultrastructure. s, sarcomere; mito, mitochondrion; Scale bar: 5 µm. (E) Quantification of ventricle area to fish length (VA/BL) index, which was used as a measurement of the cardiomegaly. 10 control fish and 5 Zfpm1^-/-fish were examined. (F) Quantification of red blood cell flow rate, which was used as a measurement of the cardiac function. 8 control fish and 7 Zfpm1^-/- fish were examined. (G) Quantification of trabecular thickness at 60 dpf. (H) Quantification of the complexity of trabecular myocardium layer at 60 dpf. G to H, 12 sections from 3 wt and 12 sections from 3 Zfpm1^-/- fish were examined. E to H, data are mean ± s.e.m. (I) Quantification of cardiomyocyte cell size in control and Zfpm1^{-/ -} fish. The surface area of individual cardiomyocyte was plotted. Sections from 3 fish for each genotype were examined. n.s: not significant. * p < 0.05. ** p < 0.01. *** p < 0.001.