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Tbx5 maintains atrial identity in post-natal cardiomyocytes by regulating an atrial-specific enhancer network. | LitMetric

AI Article Synopsis

  • Understanding how heart chambers work distinctly is crucial for treating related diseases.
  • Researchers knocked out a specific transcription factor in atrial heart cells to see its role in maintaining atrial identity.
  • The study found that the transcription factor TBX5 helps regulate atrial gene expression by binding to specific DNA regions, ensuring the proper chromatin structure for atrial function.

Article Abstract

Understanding how the atrial and ventricular heart chambers maintain distinct identities is a prerequisite for treating chamber-specific diseases. Here, we selectively knocked out (KO) the transcription factor in the atrial working myocardium to evaluate its requirement for atrial identity. Atrial inactivation downregulated atrial cardiomyocyte (aCM) selective gene expression. Using concurrent single nucleus transcriptome and open chromatin profiling, genomic accessibility differences were identified between control and KO aCMs, revealing that 69% of the control-enriched ATAC regions were bound by TBX5. Genes associated with these regions were downregulated in KO aCMs, suggesting they function as TBX5-dependent enhancers. Comparing enhancer chromatin looping using H3K27ac HiChIP identified 510 chromatin loops sensitive to TBX5 dosage, and 74.8% of control-enriched loops contained anchors in control-enriched ATAC regions. Together, these data demonstrate TBX5 maintains the atrial gene expression program by binding to and preserving the tissue-specific chromatin architecture of atrial enhancers.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10854392PMC
http://dx.doi.org/10.1038/s44161-023-00334-7DOI Listing

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