fig7

Figure 7. Effect of suppression or activation of β-catenin in cardiac myocytes on cardiac size and rhythm. (A) Gross morphology of the mouse hearts. (B) Heart weight/body weight ratio in the experimental groups at 4 weeks of age. (C) Representative immunofluorescence panels of myocardial sections stained for wheat germ agglutinin (WGA) and counterstained with DAPI. (D) Panels showing thin myocardial sections stained for PCM1 to identify cardiac myocytes. (E) Quantitation of myocyte cross-sectional area (CSA), corrected for the number of PCM1-stained cardiac myocytes, in the experimental groups showing a significant increase in the myocyte CSA in the Myh6-Mcm:Ctnnb1^GoF (GoF) hearts (n = 5). (F) Transcript levels of genes involved in determining cardiac size and function in wild type, Myh6-Mcm:Ctnnb1^LoF and Myh6-Mcm:Ctnnb1^GoF myocytes, quantitated by RT-PCR (n = 5). (G) Representative 2-lead rhythm monitoring strips in the 4 weeks old mice obtained from the surface electrocardiographic recordings in the experimental groups. PCM1: Pericentriolar material protein 1; Myh6-Mcm: myosin heavy chain 6-MerCreMer; RT-PCR: reverse transcription-polymerase chain reaction.