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Pitx2 determines left–right asymmetry of internal organs in vertebrates

Author

Listed:
  • Aimee K. Ryan

    (Howard Hughes Medical Institute, University of California)

  • Bruce Blumberg

    (The Salk Institute)

  • Concepción Rodriguez-Esteban

    (The Salk Institute)

  • Sayuri Yonei-Tamura

    (The Salk Institute)

  • Koji Tamura

    (The Salk Institute)

  • Tohru Tsukui

    (The Salk Institute)

  • Jennifer de la Peña

    (The Salk Institute)

  • Walid Sabbagh

    (The Salk Institute)

  • Jason Greenwald

    (The Salk Institute)

  • Senyon Choe

    (The Salk Institute)

  • Dominic P. Norris

    (Harvard University)

  • Elizabeth J. Robertson

    (Harvard University)

  • Ronald M. Evans

    (Howard Hughes Medical Institute
    The Salk Institute)

  • Michael G. Rosenfeld

    (Howard Hughes Medical Institute, University of California)

  • Juan Carlos Izpisúa Belmonte

    (The Salk Institute)

Abstract

The handedness of visceral organs is conserved among vertebrates and is regulated by asymmetric signals relayed by molecules such as Shh, Nodal and activin. The gene Pitx2 is expressed in the left lateral plate mesoderm and, subsequently, in the left heart and gut of mouse, chick and Xenopus embryos. Misexpression of Shh and Nodal induces Pitx2 expression, whereas inhibition of activin signalling blocks it. Misexpression of Pitx2 alters the relative position of organs and the direction of body rotation in chick and Xenopus embryos. Changes in Pitx2 expression are evident in mouse mutants with laterality defects. Thus, Pitx2 seems to serve as a critical downstream transcription target that mediates left–right asymmetry in vertebrates.

Suggested Citation

  • Aimee K. Ryan & Bruce Blumberg & Concepción Rodriguez-Esteban & Sayuri Yonei-Tamura & Koji Tamura & Tohru Tsukui & Jennifer de la Peña & Walid Sabbagh & Jason Greenwald & Senyon Choe & Dominic P. Norr, 1998. "Pitx2 determines left–right asymmetry of internal organs in vertebrates," Nature, Nature, vol. 394(6693), pages 545-551, August.
    • Handle: RePEc:nat:nature:v:394:y:1998:i:6693:d:10.1038_29004
    DOI: 10.1038/29004
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    Cited by:

    1. Manon Baudic & Hiroshige Murata & Fernanda M. Bosada & Uirá Souto Melo & Takanori Aizawa & Pierre Lindenbaum & Lieve E. Maarel & Amaury Guedon & Estelle Baron & Enora Fremy & Adrien Foucal & Taisuke I, 2024. "TAD boundary deletion causes PITX2-related cardiac electrical and structural defects," Nature Communications, Nature, vol. 15(1), pages 1-15, December.

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