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EphrinB2 affects apical constriction in Xenopus embryos and is regulated by ADAM10 and flotillin-1

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  • Yon Ju Ji

    (Laboratory of Cell and Developmental Signaling, National Cancer Institute-Frederick)

  • Yoo-Seok Hwang

    (Laboratory of Cell and Developmental Signaling, National Cancer Institute-Frederick)

  • Kathleen Mood

    (Laboratory of Cell and Developmental Signaling, National Cancer Institute-Frederick)

  • Hee-Jun Cho

    (Laboratory of Cell and Developmental Signaling, National Cancer Institute-Frederick)

  • Hyun-Shik Lee

    (ABRC, CMRI, School of Life Sciences, College of Natural Sciences, Kyungpook National University)

  • Emily Winterbottom

    (Laboratory of Cell and Developmental Signaling, National Cancer Institute-Frederick)

  • Hélène Cousin

    (University of Massachusetts)

  • Ira O. Daar

    (Laboratory of Cell and Developmental Signaling, National Cancer Institute-Frederick)

Abstract

The Eph/ephrin signalling pathways have a critical function in cell adhesion and repulsion, and thus play key roles in various morphogenetic events during development. Here we show that a decrease in ephrinB2 protein causes neural tube closure defects during Xenopus laevis embryogenesis. Such a decrease in ephrinB2 protein levels is observed on the loss of flotillin-1 scaffold protein, a newly identified ephrinB2-binding partner. This dramatic decline in ephrinB2 protein levels on the absence of flotillin-1 expression is specific, and is partly the result of an increased susceptibility to cleavage by the metalloprotease ADAM10. These findings indicate that flotillin-1 regulates ephrinB2 protein levels through ADAM10, and is required for appropriate neural tube morphogenesis in the Xenopus embryo.

Suggested Citation

  • Yon Ju Ji & Yoo-Seok Hwang & Kathleen Mood & Hee-Jun Cho & Hyun-Shik Lee & Emily Winterbottom & Hélène Cousin & Ira O. Daar, 2014. "EphrinB2 affects apical constriction in Xenopus embryos and is regulated by ADAM10 and flotillin-1," Nature Communications, Nature, vol. 5(1), pages 1-15, May.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4516
    DOI: 10.1038/ncomms4516
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