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The chromatin regulator Ankrd11 controls cardiac neural crest cell-mediated outflow tract remodeling and heart function

Author

Listed:
  • Yana Kibalnyk

    (University of Alberta
    University of Alberta)

  • Elia Afanasiev

    (McGill University)

  • Ronan M. N. Noble

    (University of Alberta
    University of Alberta)

  • Adrianne E. S. Watson

    (University of Alberta
    University of Alberta)

  • Irina Poverennaya

    (Medical University of Vienna)

  • Nicole L. Dittmann

    (University of Alberta
    University of Alberta)

  • Maria Alexiou

    (University of Alberta)

  • Kara Goodkey

    (University of Alberta
    University of Alberta)

  • Amanda A. Greenwell

    (University of Alberta
    University of Alberta, Edmonton, Alberta)

  • John R. Ussher

    (University of Alberta
    University of Alberta, Edmonton, Alberta)

  • Igor Adameyko

    (Medical University of Vienna
    Karolinska Institutet)

  • James Massey

    (Vizgen Inc.)

  • Daniel Graf

    (University of Alberta
    University of Alberta
    University of Alberta)

  • Stephane L. Bourque

    (University of Alberta
    University of Alberta)

  • Jo Anne Stratton

    (McGill University)

  • Anastassia Voronova

    (University of Alberta
    University of Alberta
    University of Alberta
    University of Alberta)

Abstract

ANKRD11 (Ankyrin Repeat Domain 11) is a chromatin regulator and a causative gene for KBG syndrome, a rare developmental disorder characterized by multiple organ abnormalities, including cardiac defects. However, the role of ANKRD11 in heart development is unknown. The neural crest plays a leading role in embryonic heart development, and its dysfunction is implicated in congenital heart defects. We demonstrate that conditional knockout of Ankrd11 in the murine embryonic neural crest results in persistent truncus arteriosus, ventricular dilation, and impaired ventricular contractility. We further show these defects occur due to aberrant cardiac neural crest cell organization leading to outflow tract septation failure. Lastly, knockout of Ankrd11 in the neural crest leads to impaired expression of various transcription factors, chromatin remodelers and signaling pathways, including mTOR, BMP and TGF-β in the cardiac neural crest cells. In this work, we identify Ankrd11 as a regulator of neural crest-mediated heart development and function.

Suggested Citation

  • Yana Kibalnyk & Elia Afanasiev & Ronan M. N. Noble & Adrianne E. S. Watson & Irina Poverennaya & Nicole L. Dittmann & Maria Alexiou & Kara Goodkey & Amanda A. Greenwell & John R. Ussher & Igor Adameyk, 2024. "The chromatin regulator Ankrd11 controls cardiac neural crest cell-mediated outflow tract remodeling and heart function," Nature Communications, Nature, vol. 15(1), pages 1-20, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-48955-1
    DOI: 10.1038/s41467-024-48955-1
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    References listed on IDEAS

    as
    1. Liu Yang & Linqing Miao & Feisi Liang & Haoliang Huang & Xiuyin Teng & Shaohua Li & Jaloliddin Nuriddinov & Michael E. Selzer & Yang Hu, 2014. "The mTORC1 effectors S6K1 and 4E-BP play different roles in CNS axon regeneration," Nature Communications, Nature, vol. 5(1), pages 1-7, December.
    2. Meng Zhang & Stephen W. Eichhorn & Brian Zingg & Zizhen Yao & Kaelan Cotter & Hongkui Zeng & Hongwei Dong & Xiaowei Zhuang, 2021. "Spatially resolved cell atlas of the mouse primary motor cortex by MERFISH," Nature, Nature, vol. 598(7879), pages 137-143, October.
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