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Spatiotemporal regulation of the GPCR activity of BAI3 by C1qL4 and Stabilin-2 controls myoblast fusion

Author

Listed:
  • Noumeira Hamoud

    (Institut de Recherches Cliniques de Montréal (IRCM)
    Université de Montréal)

  • Viviane Tran

    (Institut de Recherches Cliniques de Montréal (IRCM)
    Université de Montréal)

  • Takahiro Aimi

    (Keio University School of Medicine
    Japan Science and Technology Agency (JT))

  • Wataru Kakegawa

    (Keio University School of Medicine
    Japan Science and Technology Agency (JT))

  • Sylvie Lahaie

    (Institut de Recherches Cliniques de Montréal (IRCM)
    McGill University)

  • Marie-Pier Thibault

    (Institut de Recherches Cliniques de Montréal (IRCM))

  • Ariane Pelletier

    (Institut de Recherches Cliniques de Montréal (IRCM))

  • G. William Wong

    (Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine)

  • In-San Kim

    (Korea Institute Science and Technology
    Korea University)

  • Artur Kania

    (Institut de Recherches Cliniques de Montréal (IRCM)
    McGill University
    McGill University)

  • Michisuke Yuzaki

    (Keio University School of Medicine
    Japan Science and Technology Agency (JT))

  • Michel Bouvier

    (Université de Montréal
    Université de Montréal)

  • Jean-François Côté

    (Institut de Recherches Cliniques de Montréal (IRCM)
    Université de Montréal
    Université de Montréal
    McGill University)

Abstract

Myoblast fusion is tightly regulated during development and regeneration of muscle fibers. BAI3 is a receptor that orchestrates myoblast fusion via Elmo/Dock1 signaling, but the mechanisms regulating its activity remain elusive. Here we report that mice lacking BAI3 display small muscle fibers and inefficient muscle regeneration after cardiotoxin-induced injury. We describe two proteins that repress or activate BAI3 in muscle progenitors. We find that the secreted C1q-like1–4 proteins repress fusion by specifically interacting with BAI3. Using a proteomic approach, we identify Stabilin-2 as a protein that interacts with BAI3 and stimulates its fusion promoting activity. We demonstrate that Stabilin-2 activates the GPCR activity of BAI3. The resulting activated heterotrimeric G-proteins contribute to the initial recruitment of Elmo proteins to the membrane, which are then stabilized on BAI3 through a direct interaction. Collectively, our results demonstrate that the activity of BAI3 is spatiotemporally regulated by C1qL4 and Stabilin-2 during myoblast fusion.

Suggested Citation

  • Noumeira Hamoud & Viviane Tran & Takahiro Aimi & Wataru Kakegawa & Sylvie Lahaie & Marie-Pier Thibault & Ariane Pelletier & G. William Wong & In-San Kim & Artur Kania & Michisuke Yuzaki & Michel Bouvi, 2018. "Spatiotemporal regulation of the GPCR activity of BAI3 by C1qL4 and Stabilin-2 controls myoblast fusion," Nature Communications, Nature, vol. 9(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-06897-5
    DOI: 10.1038/s41467-018-06897-5
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    Cited by:

    1. Viviane Tran & Sarah Nahlé & Amélie Robert & Inès Desanlis & Ryan Killoran & Sophie Ehresmann & Marie-Pier Thibault & David Barford & Kodi S. Ravichandran & Martin Sauvageau & Matthew J. Smith & Marie, 2022. "Biasing the conformation of ELMO2 reveals that myoblast fusion can be exploited to improve muscle regeneration," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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