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. 2021 Jul 16;12:712666. doi: 10.3389/fphys.2021.712666

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Copyright © 2021 Mandla, Jung and Vedantham.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Sinoatrial node hypoplasia and dysfunction after deletion of a key pacemaker cell-specific enhancer. (A) Three-dimensional reconstruction of light sheet fluorescence image of Hcn4 + sinoatrial node (san, green), right atrium (pink, ra) and superior vena cava (gray, svc) from a WT control adult heart (left) in comparison to (B) a heart obtained from a littermate lacking both copies of an SAN-specific enhancer (ISE) for the transcription factor Isl1. Hearts were stained in whole mount with Hcn4 antibody and san, ra, and svc were manually segmented. Note the markedly reduced size of the Hcn4 + SAN in the Isl1^Δ^ISE/Δ^ISE heart. (C) Electrocardiograms recorded from a WT control adult mouse (left) and (D) an Isl1^Δ^ISE/Δ^ISE littermate demonstrate an example of sinus arrhythmias in animals lacking the Isl1 enhancer.