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Live imaging molecular changes in junctional tension upon VE-cadherin in zebrafish

Author

Listed:
  • Anne Karine Lagendijk

    (Institute for Molecular Bioscience, Genomics of Development and Disease division, The University of Queensland)

  • Guillermo A. Gomez

    (The University of Queensland
    SA Pathology and the University of South Australia)

  • Sungmin Baek

    (Institute for Molecular Bioscience, Genomics of Development and Disease division, The University of Queensland)

  • Daniel Hesselson

    (Garvan Institute of Medical Research)

  • William E. Hughes

    (Garvan Institute of Medical Research)

  • Scott Paterson

    (Institute for Molecular Bioscience, Genomics of Development and Disease division, The University of Queensland)

  • Daniel E. Conway

    (Virginia Commonwealth University)

  • Heinz-Georg Belting

    (Biozentrum der Universität Basel)

  • Markus Affolter

    (Biozentrum der Universität Basel)

  • Kelly A. Smith

    (Institute for Molecular Bioscience, Genomics of Development and Disease division, The University of Queensland)

  • Martin A. Schwartz

    (Yale University School of Medicine)

  • Alpha S. Yap

    (The University of Queensland)

  • Benjamin M. Hogan

    (Institute for Molecular Bioscience, Genomics of Development and Disease division, The University of Queensland)

Abstract

Forces play diverse roles in vascular development, homeostasis and disease. VE-cadherin at endothelial cell-cell junctions links the contractile acto-myosin cytoskeletons of adjacent cells, serving as a tension-transducer. To explore tensile changes across VE-cadherin in live zebrafish, we tailored an optical biosensor approach, originally established in vitro. We validate localization and function of a VE-cadherin tension sensor (TS) in vivo. Changes in tension across VE-cadherin observed using ratio-metric or lifetime FRET measurements reflect acto-myosin contractility within endothelial cells. Furthermore, we apply the TS to reveal biologically relevant changes in VE-cadherin tension that occur as the dorsal aorta matures and upon genetic and chemical perturbations during embryonic development.

Suggested Citation

  • Anne Karine Lagendijk & Guillermo A. Gomez & Sungmin Baek & Daniel Hesselson & William E. Hughes & Scott Paterson & Daniel E. Conway & Heinz-Georg Belting & Markus Affolter & Kelly A. Smith & Martin A, 2017. "Live imaging molecular changes in junctional tension upon VE-cadherin in zebrafish," Nature Communications, Nature, vol. 8(1), pages 1-12, December.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01325-6
    DOI: 10.1038/s41467-017-01325-6
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    Cited by:

    1. Jianmin Yin & Niels Schellinx & Ludovico Maggi & Kathrin Gundel & Cora Wiesner & Maria Paraskevi Kotini & Minkyoung Lee & Li-Kun Phng & Heinz-Georg Belting & Markus Affolter, 2024. "Initiation of lumen formation from junctions via differential actomyosin contractility regulated by dynamic recruitment of Rasip1," Nature Communications, Nature, vol. 15(1), pages 1-18, December.

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