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Tbx5a lineage tracing shows cardiomyocyte plasticity during zebrafish heart regeneration

Author

Listed:
  • Héctor Sánchez-Iranzo

    (Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII))

  • María Galardi-Castilla

    (Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII))

  • Carolina Minguillón

    (CSIC-Institut de Biologia Molecular de Barcelona Parc Científic de Barcelona C/ Baldiri i Reixac
    Barcelonabeta Brain Research Center, Pasqual Maragall Foundation)

  • Andrés Sanz-Morejón

    (Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII)
    University of Bern)

  • Juan Manuel González-Rosa

    (Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII)
    Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School)

  • Anastasia Felker

    (University of Zürich)

  • Alexander Ernst

    (University of Bern)

  • Gabriela Guzmán-Martínez

    (Hospital Universitario La Paz, IdiPAZ)

  • Christian Mosimann

    (University of Zürich)

  • Nadia Mercader

    (Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII)
    University of Bern)

Abstract

During development, mesodermal progenitors from the first heart field (FHF) form a primitive cardiac tube, to which progenitors from the second heart field (SHF) are added. The contribution of FHF and SHF progenitors to the adult zebrafish heart has not been studied to date. Here we find, using genetic tbx5a lineage tracing tools, that the ventricular myocardium in the adult zebrafish is mainly derived from tbx5a+ cells, with a small contribution from tbx5a− SHF progenitors. Notably, ablation of ventricular tbx5a+-derived cardiomyocytes in the embryo is compensated by expansion of SHF-derived cells. In the adult, tbx5a expression is restricted to the trabeculae and excluded from the outer cortical layer. tbx5a-lineage tracing revealed that trabecular cardiomyocytes can switch their fate and differentiate into cortical myocardium during adult heart regeneration. We conclude that a high degree of cardiomyocyte cell fate plasticity contributes to efficient regeneration.

Suggested Citation

  • Héctor Sánchez-Iranzo & María Galardi-Castilla & Carolina Minguillón & Andrés Sanz-Morejón & Juan Manuel González-Rosa & Anastasia Felker & Alexander Ernst & Gabriela Guzmán-Martínez & Christian Mosim, 2018. "Tbx5a lineage tracing shows cardiomyocyte plasticity during zebrafish heart regeneration," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02650-6
    DOI: 10.1038/s41467-017-02650-6
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    Cited by:

    1. Yu Xia & Sierra Duca & Björn Perder & Friederike Dündar & Paul Zumbo & Miaoyan Qiu & Jun Yao & Yingxi Cao & Michael R. M. Harrison & Lior Zangi & Doron Betel & Jingli Cao, 2022. "Activation of a transient progenitor state in the epicardium is required for zebrafish heart regeneration," Nature Communications, Nature, vol. 13(1), pages 1-18, December.
    2. Carmen Sena-Tomás & Angelika G. Aleman & Caitlin Ford & Akriti Varshney & Di Yao & Jamie K. Harrington & Leonor Saúde & Mirana Ramialison & Kimara L. Targoff, 2022. "Activation of Nkx2.5 transcriptional program is required for adult myocardial repair," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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