Fig. 3.

KCNQ mutants exhibit early onset of prolonged, fibrillatory contractions. (A) Systolic interval lengths for all heartbeats in each record were computed and averaged for each fly (∗, P < 0.05, analysis of covariance regression analysis and independent samples t test). (B) Incidence of fibrillation, plotted as a percentage of total flies (∗, P < 0.05, Pearson's χ² test). For A and B, ◇, WT; □, KCNQ¹⁸⁶; ▵, KCNQ³⁷⁰; n = 20–30 flies per data point. (C) Arrhythmicity index from semiintact fly heart preparations in 3-week-old flies. Overexpression of the WT UAS-KCNQ in KCNQ mutant flies (dark blue/red bars) significantly reduced the arrhythmicity index compared with control flies with the UAS-KCNQ construct or the 24B driver alone (light blue/red bars; ∗, P < 0.05). (D) Combined data, showing the distribution of systolic intervals for control and KCNQ mutant flies. Systolic intervals lasting >1.5 s were grouped together and are shown in the last bar of each histogram. The bottom row of the histograms shows rescue of the 3-week-old KCNQ¹⁸⁶ mutant phenotype by overexpression of KCNQ transgene in all mesoderm (on the left) and improvement in the cardiac status of 7-week-old WT flies by overexpression of KCNQ transgene specifically in all cardiomyocytes (right) using the GMH5 driver (17).