Research Paper Volume 7, Issue 9 pp 648—660

Heart-specific Rpd3 downregulation enhances cardiac function and longevity


Figure 5. Overall heart function is enhanced by heart-specific Rpd3 downregulation. (A) Oxidative stress tolerance between the 2-day-old male flies of two of single transgene controls (+/tinG4, rpd3Ri/+) and heart-specific Rpd3 downregulation (rpd3Ri/tinG4), which was made with the mean ± SEM over two independent assays. The survivorship (A) and heart rate (B) were measured across the same time points (0, 18, 24, and 42 hours). (B) The corresponding heart rates during the aforementioned oxidative stress test (A). More than 20 heart rates were measured at each time point. HBM: heart beat per minute. (C) Comparison of heart- and eye-specific Rpd3 downregulation (four independent assays). Left: The percent change of heart rate from the common control rpd3Ri/+ (0%) at each time point, which was calculated from the heart rate graphs (B). Only heart-specific Rpd3 downregulation displayed a statistically significant cardiovascular enhancement (p < 0.0001) compared to eye-specific downregulation (p = 0.94) from the control (rpd3Ri/+). Right: The differences in survivorship (%) for the oxidative stress test when compared to the common control rpd3Ri/+ (0%). The percentages were calculated from the four different time points (p = 0.03 - 0.0001) of the survival curves (A). (D) Comparison of oxidative stress resistance after 24 hours paraquat treatment among the +/tinG4, Rpd3Ri/+ single transgene controls and heart-specific (rpd3Ri/tinG4), eye-specific (rpd3Ri/GMRG4) Rpd3 downregulations. The survivorship percentage (%) at 24 hours was assessed as mean ± SEM over 5 - 7 independent stress assays. (E) The heart failure rate measured at 24 hours of oxidative stress (A) in 3 - 8 repeat experiments using a total of 22 - 134 flies. (F) The heart recovery rate measured at 24 hours of oxidative stress (A) in 5 repeat trials with a total of 66 - 67 flies.