Reprogramming to a Conduction-like Phenotype in Vivo is Dependent on Canonical Notch Signaling. (A) RT-qPCR analysis of Hcn1 gene expression changes within the mid-ventricular region of Notch activated hearts, with and without downstream inactivation of canonical Notch signaling via DNMAML (Mlc2vCre/+; NICD versus Mlc2vCre/+; NICD/DNMAML). Hcn1 levels are nearly 8-fold upregulated with Notch activation, however in the presence of DNMAML, Hcn1 levels are significantly reduced. This suggests that the effects of Notch activation to promote a conduction-like phenotype are largely MAML-dependent and therefore mediated by canonical Notch signaling. Control mice are NICD or NICD/DNMAML littermates. n=9 control, n=8 Mlc2vCre/+; NICD, n=6 Mlc2vCre/+; NICD/DNMAML. Data are expressed as mean ± SEM. Group comparison was performed using a one-way ANOVA and Tukey-Kramer test for post-hoc analysis. *p<0.05