Extended Data Figure 6. Quantitation of Cre activity and DNA recombination in the hearts of Kit^+/MCM × R-GFP mice.

a, Time line for tamoxifen administration in Kit^+/MCM × R-GFP mice. b, PCR from DNA generated from the bone marrow (BM), whole heart or semi-purified cardiomyocytes after 6 weeks of tamoxifen treatment in Kit^+/MCM × R-GFP mice (n=2). Bone marrow shows most of the DNA as having been recombined by Cre, while whole heart is just barely discernable, and purified cardiomyocytes show essentially no recombination given the sensitivity constraints of this assay. c, qPCR was also run to more sensitively detect and quantify the extent of recombination, which was set relative to the recombination in bone marrow. Semi-purified cardiomyocytes (CM) showed very low rates. Averaged data are shown and error bars are s.e.m. of duplicate technical replicates from n=3 Kit^+/MCM × R-GFP mice. d, Schematic of the tamoxifen time course and timing of myocardial infarction (MI) in Kit^+/MCM × R-GFP mice. e, Echocardiography measured cardiac fractional shortening (FS%) was assessed in the mice after MI, which shows a reduction in cardiac ventricular performance at 1, 2 and 4 weeks after injury. The number of mice analyzed is shown in the bars. Error bars represent the s.e.m. Both the control and experimental groups showed an equivalent reduction in cardiac function post-MI. f, Images of dissociated cardiomyocytes from hearts of Kit^+/MCM × R-GFP mice 4 weeks after MI, which were fixed and stained for sarcomeric α-actin antibody (red) and eGFP (green) at 2 different magnifications. One eGFP⁺ cardiomyocyte is shown with sarcomeric patterning of the eGFP fluorescence.