Research Paper Volume 7, Issue 9 pp 648—660

Heart-specific Rpd3 downregulation enhances cardiac function and longevity


Figure 6. Stress resistance and heart function are reduced by heart-specific Rpd3 upregulation. (A) Heat-stress survivorship of flies with heart-specific Rpd3 upregulation of wild-type (WT), and non-phosphorylated mutant (ADA: S419A/S421A). The p-value (p<0.03, log-rank test) between +/tinG4 and rpd3WT/tinG4 indicates that heat resistance is significantly diminished with increased rpd3WT expression. The p-value between rpd3WT/tinG4 and rpd3ADA/tinG4 shows a more significant difference (p<0.0001). (B) The corresponding heart rates during the aforementioned heat stress test (A) across the same time points (0, 18, and 24 hours). At each time point, more than 20 heart rates were measured. (C) Change of survivorship and heart rates of heart-specific Rpd3 upregulation under heat stress. Changed percentages (parenthesis) of the median survival time of Rpd3WT (or ADA) upregulation (5 independent experiments) were normalized with that of the common control (+/tinG4). The changes in heart rate between the +/tinG4 and Rpd3 upregulations are represented as the average of three time points (0, 18, and 24 hours) in the heart rate graphs (B).