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A mechanosensitive Ca2+ channel activity is dependent on the developmental regulator DEK1

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  • Daniel Tran

    (Université de Lyon, ENS de Lyon, UCB Lyon 1, CNRS, INRA
    Université Paris-Sud, Sciences Plant Saclay
    McGill University)

  • Roberta Galletti

    (Université de Lyon, ENS de Lyon, UCB Lyon 1, CNRS, INRA)

  • Enrique D. Neumann

    (Université de Lyon, ENS de Lyon, UCB Lyon 1, CNRS, INRA)

  • Annick Dubois

    (Université de Lyon, ENS de Lyon, UCB Lyon 1, CNRS, INRA)

  • Reza Sharif-Naeini

    (McGill University)

  • Anja Geitmann

    (McGill University)

  • Jean-Marie Frachisse

    (Université Paris-Sud, Sciences Plant Saclay)

  • Olivier Hamant

    (Université de Lyon, ENS de Lyon, UCB Lyon 1, CNRS, INRA)

  • Gwyneth C. Ingram

    (Université de Lyon, ENS de Lyon, UCB Lyon 1, CNRS, INRA)

Abstract

Responses of cells to mechanical stress are thought to be critical in coordinating growth and development. Consistent with this idea, mechanically activated channels play important roles in animal development. For example, the PIEZO1 channel controls cell division and epithelial-layer integrity and is necessary for vascular development in mammals. In plants, the actual contribution of mechanoperception to development remains questionable because very few putative mechanosensors have been identified and the phenotypes of the corresponding mutants are rather mild. Here, we show that the Arabidopsis Defective Kernel 1 (DEK1) protein, which is essential for development beyond early embryogenesis, is associated with a mechanically activated Ca2+ current in planta, suggesting that perception of mechanical stress plays a critical role in plant development.

Suggested Citation

  • Daniel Tran & Roberta Galletti & Enrique D. Neumann & Annick Dubois & Reza Sharif-Naeini & Anja Geitmann & Jean-Marie Frachisse & Olivier Hamant & Gwyneth C. Ingram, 2017. "A mechanosensitive Ca2+ channel activity is dependent on the developmental regulator DEK1," Nature Communications, Nature, vol. 8(1), pages 1-8, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00878-w
    DOI: 10.1038/s41467-017-00878-w
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