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. 2015 Jan 15;4:e04801. doi: 10.7554/eLife.04801

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© 2014, Shimizu 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 7. — (A) MCU and MICU1 are expressed in the developing zebrafish hearts (arrowhead). (B) Overexpression of MCU is sufficient to restore coordinated cardiac contractions in tre embryos (47.1 ± 1.6% embryos, n = 112 as opposed to 18.3 ± 5.3% of uninjected siblings, n = 64) while this effect is significantly attenuated when co-injected with morpholino antisense oligonucleotide targeted to VDAC2 (27.1 ± 1.9% embryos, n = 135). (C) Suboptimal overexpression of MCU (MCU^S) and VDAC2 (VDAC2^S) in combination is able to suppress cardiac fibrillation in tre embryos (42.9 ± 2.6% embryos, n = 129). (D) The ability of VDAC2 to restore rhythmic contractions in tre embryos (48.5 ± 3.5% embryos, n = 111) is significantly attenuated when MCU is knocked down by antisense oligonucleotide (MO^MCU) (25.6 ± 2.4% embryos, n = 115). (E) Overexpression of MICU1 is sufficient to restore rhythmic cardiac contractions in tre embryos (49.3 ± 3.4% embryos, n = 127 compared to 16.8 ± 1.4% of uninjected siblings, n = 150). This effect is abrogated by VDAC2 knockdown (MO^VDAC2, 25.3 ± 5.5% embryos, n = 97). (F) Suboptimal overexpression of MICU1 (MICU1^S) and VDAC2 (VDAC2^S) in combination is able to restore rhythmic cardiac contractions in tre embryos (48.6 ± 6.0%, n = 106). Error bars represent s.d.; *p < 0.05; ***p < 0.001.

DOI: http://dx.doi.org/10.7554/eLife.04801.027

Figure 7—figure supplement 1. — (A) MCU and MICU1 are expressed in the developing zebrafish hearts (arrowhead). (B) Overexpression of MCU is sufficient to restore coordinated cardiac contractions in tre embryos (47.1 ± 1.6% embryos, n = 112 as opposed to 18.3 ± 5.3% of uninjected siblings, n = 64) while this effect is significantly attenuated when co-injected with morpholino antisense oligonucleotide targeted to VDAC2 (27.1 ± 1.9% embryos, n = 135). (C) Suboptimal overexpression of MCU (MCU^S) and VDAC2 (VDAC2^S) in combination is able to suppress cardiac fibrillation in tre embryos (42.9 ± 2.6% embryos, n = 129). (D) The ability of VDAC2 to restore rhythmic contractions in tre embryos (48.5 ± 3.5% embryos, n = 111) is significantly attenuated when MCU is knocked down by antisense oligonucleotide (MO^MCU) (25.6 ± 2.4% embryos, n = 115). (E) Overexpression of MICU1 is sufficient to restore rhythmic cardiac contractions in tre embryos (49.3 ± 3.4% embryos, n = 127 compared to 16.8 ± 1.4% of uninjected siblings, n = 150). This effect is abrogated by VDAC2 knockdown (MO^VDAC2, 25.3 ± 5.5% embryos, n = 97). (F) Suboptimal overexpression of MICU1 (MICU1^S) and VDAC2 (VDAC2^S) in combination is able to restore rhythmic cardiac contractions in tre embryos (48.6 ± 6.0%, n = 106). Error bars represent s.d.; *p < 0.05; ***p < 0.001.

DOI: http://dx.doi.org/10.7554/eLife.04801.027