Motivated by a CRISPR screen, in vitro and in vivo studies identified an essential role for the bromodomain and extraterminal domain (BET) family member BRD4 in the differentiation of second heart field progenitors into cardiomyocytes. Single-cell transcriptomic studies showed that BRD4 deficiency affects a specific subset of cardiac progenitor cells.
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References
Padmanabhan, A. et al. BRD4 (bromodomain-containing protein 4) interacts with GATA4 (GATA binding protein 4) to govern mitochondrial homeostasis in adult cardiomyocytes. Circulation 142, 2338–2355 (2020). This paper shows how BRD4 interacts with tissue-specific transcription factors to mediate cardiomyocyte homeostasis.
Linares-Saldana, R. et al. BRD4 orchestrates genome folding to promote neural crest differentiation. Nat. Genet. 53, 1480–1492 (2021). This paper elucidates the role of BRD4 in mediating genome folding and its consequences for neural crest differentiation.
Padmanabhan, A. & Haldar, S. M. Drugging transcription in heart failure. J. Physiol. 598, 3005–3014 (2020). A review article that discusses the therapeutic potential of BET inhibitors.
Kwon, C. et al. Canonical Wnt signaling is a positive regulator of mammalian cardiac progenitors. Proc. Natl Acad. Sci. USA 104, 10894–10899 (2007). This paper reports that WNT signaling is necessary for maintaining cardiac progenitor cells.
Morton, S. U., Quiat, D., Seidman, J. G. & Seidman, C. E. Genomic frontiers in congenital heart disease. Nat. Rev. Cardiol. 19, 26–42 (2022). A review article that highlights advances in genomic understanding of congenital heart disease.
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This is a summary of: Padmanabhan, A. et al. A genome-wide CRISPR screen identifies BRD4 as a regulator of cardiomyocyte differentiation. Nat. Cardiovasc. Res. https://doi.org/10.1038/s44161-024-00431-1 (2024).
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Taking BETs on cardiomyocyte differentiation. Nat Cardiovasc Res 3, 265–266 (2024). https://doi.org/10.1038/s44161-024-00443-x
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DOI: https://doi.org/10.1038/s44161-024-00443-x
