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. 2018 Oct 23;8:15642. doi: 10.1038/s41598-018-33958-y

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Role of the TBX5-PITX2 regulatory loop in spontaneous depolarization generation. (a) Cytosolic calcium concentration ([Ca²⁺]_i) and action potential (AP) characteristics in homozygous TBX5-knockout (Hom-Tbx5), heterozygous TBX5-knockout (Het-Tbx5), homozygous PITX2-knockout (Hom-Pitx2), heterozygous PITX2-knockout (Het-Pitx2) and heterozygous knockout of both PITX2 and TBX5 (Het-Pitx2-Tbx5) atrial cells. TBX5 insufficiency (e.g., Hom-Tbx5) led to AP prolongation and diastolic calcium elevation, whereas PITX2 insufficiency (e.g., Hom-Pitx2) caused AP abbreviation and a decrease in diastolic calcium. AP abnormalities induced by TBX5 haploinsufficiency were rescued by PITX2 haploinsufficiency. (b–d) The diastolic calcium concentration (Ca_diast), resting membrane potential (RMP) and action potential duration (APD₉₀) for all cell variants were compared to control atrial myocytes (black bar).