Spatiotemporal regulation of the GPCR activity of BAI3 by C1qL4 and Stabilin-2 controls myoblast fusion
- Authors
- Hamoud, Noumeira; Tran, Viviane; Aimi, Takahiro; Kakegawa, Wataru; Lahaie, Sylvie; Thibault, Marie-Pier; Pelletier, Ariane; Wong, G. William; Kim, In-San; Kania, Artur; Yuzaki, Michisuke; Bouvier, Michel; Cote, Jean-Francois
- Issue Date
- 26-10월-2018
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- NATURE COMMUNICATIONS, v.9
- Indexed
- SCIE
SCOPUS
- Journal Title
- NATURE COMMUNICATIONS
- Volume
- 9
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/72437
- DOI
- 10.1038/s41467-018-06897-5
- ISSN
- 2041-1723
- 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.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - Graduate School > KU-KIST Graduate School of Converging Science and Technology > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.