Figure 1—figure supplement 1.

Following ventricular ablation, ventricular and atrial cardiomyocyte proliferation leads to cardiac recovery at 96 hpt. (A, B) Confocal maximum intensity projections of Tg(vmhc:mCherry-NTR) fish show extensive cell death as detected by TUNEL staining in the ventricles of (B) MTZ-treated fish when compared with (A) DMSO-treated controls at 24 hpt. (C) Quantitation of TUNEL-positive CMs in the ventricle of control (n = 15) and ablated (n = 13) fish hearts at 24 hpt confirms cell death is induced by MTZ treatment. (D, E) Confocal maximum intensity projections of Tg(cmlc2:GFP; vmhc:mCherry-NTR) fish show increased proliferation of CMs as detected by EdU⁺/cmlc2:GFP⁺ double positive staining (white arrows) in the ventricles and atria of (E) MTZ-treated fish when compared with (D) DMSO-treated controls at 48 hpt. Yellow arrows point to EdU⁺ proliferating non-cardiomyocytes. (D’, E’) Single confocal sections show EdU⁺ proliferating cells. (F) Quantitation of EdU⁺/cmlc2:GFP⁺ double positive CMs in the ventricle or atrium of control (n = 12) and ablated (n = 12) fish hearts at 48 hpt confirms increased proliferation in ventricle-ablated hearts. (G) Quantitation of ventricular area shows loss of myocardial ventricular tissue in Tg(vmhc:mCherry-NTR) MTZ-treated fish at 24 hpt (n = 12) when compared to control non-ablated fish (n = 7). At 96 hpt, Tg(vmhc:mCherry-NTR) MTZ-ablated hearts show recovery of ventricular area (n = 8, control; n = 9, ablated). (H) Quantitation of ventricular fractional area change (FAC) reveals decreased ventricular function in Tg(vmhc:mCherry-NTR) MTZ-treated fish at 24 hpt (n = 9) when compared to control non-ablated fish (n = 6). At 96 hpt, Tg(vmhc:mCherry-NTR) MTZ-ablated hearts (n = 5) dispaly comparable ventricular function to that of control hearts (n = 6). V, ventricle; A, atrium; dpf, days post-fertilization. Dashed lines outline the heart. Bars: 50 μm. (C) Mean + s.d. (F–H) Mean + s.e.m. Student’s t-test, ***, p<0.001; ns, p>0.05.