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. 2019 Mar 21;8:e41814. doi: 10.7554/eLife.41814

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© 2019, Dai et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 3. — (A) Western blot from atrial tissue from 10 animals per genotype was used to measure RyR2 expression. RyR2 was significantly decreased in Tbx5^fl/fl;R26^CreERT2 atria compared to R26^CreERT2 atria (normalized to GAPDH). (B) Fluo-4 loaded cardiomyocytes demonstrated reduced spark frequency in Tbx5^fl/fl;R26^CreERT2 compared to R26^CreERT2 atrial cardiomyocytes (representative recordings). (C) Spark frequency was reduced at rest and after steady state pacing at different frequencies (myocytes/mice; n = 12/4 Tbx5^fl/fl;R26^CreERT2 and n = 12/3 R26^CreERT2). (D) Ryanodine binding assay (without normalization) demonstrated no significant difference over the physiologic range of [Ca]_i in Tbx5^fl/fl;R26^CreERT2 compared to R26^CreERT2 (Weng et al., 2018). Each measure corresponds to an assay performed on pooled atria from 8 to 10 mice with three independent measures per condition (*p<0.05, **p<0.01, ***p<0.001).

Figure 3—source data 1. Western blot for Figure 3A.

elife-41814-fig3-data1.xlsx^{(8.5KB, xlsx)}

DOI: 10.7554/eLife.41814.013

Figure 3—source data 2. Spark analysis for Figure 3C.

elife-41814-fig3-data2.xlsx^{(12.4KB, xlsx)}

DOI: 10.7554/eLife.41814.014

Figure 3—source data 3. Ryanodine binding assay for Figure 3D.

elife-41814-fig3-data3.xlsx^{(168.7KB, xlsx)}

DOI: 10.7554/eLife.41814.015