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Fig. 2 | BMC Systems Biology

Fig. 2

From: NUP155 insufficiency recalibrates a pluripotent transcriptome with network remodeling of a cardiogenic signaling module

Fig. 2

Contractile NUP155 deficient embryoid bodies exhibit dysrhythmia. a Embryoid bodies (EBs) were loaded with Fluo4-AM to visualize Ca2+ handling during systolic and diastolic phases of contractile cycling, as indicated. Color legend to left of image identifies fluorescence of regions that range from high Ca2+ concentration in red, medium concentration in cyan, to low concentration in blue. b Ca2+ handling for each region of interest (ROI), with timescale in seconds (s) and range of fluorescent intensity units (i.u.) indicated in lower right. c, d Visualization and measurement of contractile EBs following treatment with 10 mM isoproterenol (Iso). e, f Untreated beating areas in NUP155 deficient EBs demonstrates increased frequency of contractile cycling, with variable Ca2+ handling. g, h Agonist treatment of NUP155 deficient EBs aggravates the irregular contractile cycling observed in unstimulated controls that ranged in severity from hypercontractility to loss of rhythmic contraction. I Measurement of intervals between peaks highlight a significant decrease of time between Ca2+ waves in NUP155+/− EBs compared to controls, independent of isoproterenol treatment (n = 3, *p < 0.05 vs WT Ctrl, **p < 0.05 vs WT Iso). j Changes in mean amplitude of Ca2+ waves. WT Iso treated, and NUP155+/− EBs with and without Iso treatment did not show significant differences, but were significantly decreased compared to WT Ctrl. (n = 3, *p < 0.05 vs WT Ctrl)

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