Figure 5. IDKO ACMs spontaneously proliferate. (A) IDKO hearts displayed a 32% increase in heart weight to body weight ratio (HW/BW; n = 4 per group; *, P < 0.01). (B) Relative cell size of IDKO ACMs was 5% smaller than control ACM (n = 4 per group; *, P < 0.05). CM, cardiac myocyte. (C) Immuno- fluorescence images of myocardial sections showing that IDKO ACMs reenter S phase in vivo (green, BrdU; red, troponin C; blue, DAPI). Bar, 40 µm. (D) Quantitation of BrdU labeling (n = 3 per group). *, P = 0.003 for sham-operated IDKO versus control; **, P < 0.0001 for TAC-operated IDKO versus control. (A, B, and D) Error bars represent the SEM. (E) IDKO cardiac myocytes complete cytokinesis in vitro. Histone 2B–GFP was expressed under control of the troponin T promoter (green) to visualize cardiomyocyte nuclei. The images were collected for 24 h at 15-min intervals (see Video 1). Bar, 15 µm. Interestingly, HP1- is not present at the Myc promoter, which is up-regulated in ACMs in response to hypertrophic signals. Normal cellular localization of HP1 was disrupted in IDKO car- diac myocytes (Fig. 7 D). Rb/p130 is dispensable for Suv39h1-mediated H3K9me3 The fact that IDKO cardiac myocytes demonstrated persistent H3K9me3 at E2F-dependent promoters suggested that Rb/p130 Epigenetic regulation of cardiac proliferation • Sdek et al. 415