Congenital heart defects research
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It is established that TAK1 via TAB2 and PKA-Cα is activated at the primary cilium during cardiomyogenesis and that TAK1 activation at this site is enhanced by cardiomyogenic signaling molecules, including ligands of the TGFB/BMP superfamily.
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Pathogenic variants in the genes encoding the non-canonical TGFB signaling components TAK1 (MAP3K7 ) , TAB2 and PKA-Cα (PRKACA) cause rare multisystem disorders, which may include congenital heart disease (CHD). To investigate the role of TAK1 signaling in CHD, we performed genetic analysis of CHD patients and discovered an increased burden of rare TAB2 and TAK1 variants in patients with extracardiac abnormalities. To address the mechanism of TAK1 in heart development, we performed experiments in cell and animal models. Zebrafish tak1 and tab2 mutants presented with cardiac and extracardiac developmental defects, and tak1 mutant hearts showed downregulation of genes encoding core cardiac transcription factors, sarcomeric proteins and extracellular matrix proteins. In vitro experiments indicated that TAK1 via TAB2 and PKA-Cα is activated at the primary cilium during cardiomyogenesis; activation at this site is enhanced by TGFB/BMP ligands. Inactivation of TAK1 inhibited ciliary signaling and cardiomyocyte differentiation, and patient-derived TAK1 variants reduced its ciliary localization. In conclusion, our data establish a pivotal role for TAK1 and its upstream regulators at the primary cilium in heart development and syndromic CHD.
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@article{Doanl2026TAK1,
title = {TAK1 operates at the primary cilium in non-canonical TGFB/BMP signaling to control heart development},
author = {Canan Doğanlı and Oskar Kaaber Thomsen and Daniel A. Baird and Yeasmeen Ali and Menachem V. K. Sarusie and Enrique Audain and Line Jeanett Jessen and Pauline Munck Truelsen and Johanne B. Mogensen and Maria Schrøder Holm and Kateřina Apolínová and Lorenzo Buttò and Maria Vittoria Diamanti and Jindřiška Leischner Fialová and Emma M. Wade and Stephen P. Robertson and Lotte B. Pedersen and Laurent Argiro and Fabienne Lescroart and Marc‐Phillip Hitz and Søren T. Christensen and Lars Allan Larsen},
journal = {PLoS Biology},
year = {2026},
doi = {10.1371/journal.pbio.3003902},
url = {https://doi.org/10.1371/journal.pbio.3003902}
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