Fig. 3.

Ca²⁺-dependent and Ca²⁺-independent processes contribute to impaired myocardial relaxation in mutant flies. (A) Small-molecule compounds elicited significant, incremental increases in the diameters of 3-wk-old fly hearts. Incubation with EGTA/EGTA,AM-containing AHL chelated extracellular and intracellular Ca²⁺, halted contraction, and prompted increases in heart tube diameters from baseline (i.e., diastole). Subsequent incubation with blebbistatin inhibited acto-myosin attachments, leading to further increases in cardiac diameters. (B) Ca²⁺ chelation prompted a significantly greater increase in the diameter of hearts overexpressing the TnT variants vs. WT. (C) Blebbistatin treatment caused an exaggerated response across the wall of all mutant hearts, relative to control. Data are presented as mean ± SEM (n = 20; **P ≤ 0.01; ***P ≤ 0.001; ****P ≤ 0.0001).