TY - JOUR
T1 - Cell surface flip-flop of phosphatidylserine is critical for PIEZO1-mediated myotube formation
AU - Tsuchiya, Masaki
AU - Hara, Yuji
AU - Okuda, Masaki
AU - Itoh, Karin
AU - Nishioka, Ryotaro
AU - Shiomi, Akifumi
AU - Nagao, Kohjiro
AU - Mori, Masayuki
AU - Mori, Yasuo
AU - Ikenouchi, Junichi
AU - Suzuki, Ryo
AU - Tanaka, Motomu
AU - Ohwada, Tomohiko
AU - Aoki, Junken
AU - Kanagawa, Motoi
AU - Toda, Tatsushi
AU - Nagata, Yosuke
AU - Matsuda, Ryoichi
AU - Takayama, Yasunori
AU - Tominaga, Makoto
AU - Umeda, Masato
N1 - Publisher Copyright:
© 2018 The Author(s).
PY - 2018/12/1
Y1 - 2018/12/1
N2 - Myotube formation by fusion of myoblasts and subsequent elongation of the syncytia is essential for skeletal muscle formation. However, molecules that regulate myotube formation remain elusive. Here we identify PIEZO1, a mechanosensitive Ca2+ channel, as a key regulator of myotube formation. During myotube formation, phosphatidylserine, a phospholipid that resides in the inner leaflet of the plasma membrane, is transiently exposed to cell surface and promotes myoblast fusion. We show that cell surface phosphatidylserine inhibits PIEZO1 and that the inward translocation of phosphatidylserine, which is driven by the phospholipid flippase complex of ATP11A and CDC50A, is required for PIEZO1 activation. PIEZO1-mediated Ca2+ influx promotes RhoA/ROCK-mediated actomyosin assemblies at the lateral cortex of myotubes, thus preventing uncontrolled fusion of myotubes and leading to polarized elongation during myotube formation. These results suggest that cell surface flip-flop of phosphatidylserine acts as a molecular switch for PIEZO1 activation that governs proper morphogenesis during myotube formation.
AB - Myotube formation by fusion of myoblasts and subsequent elongation of the syncytia is essential for skeletal muscle formation. However, molecules that regulate myotube formation remain elusive. Here we identify PIEZO1, a mechanosensitive Ca2+ channel, as a key regulator of myotube formation. During myotube formation, phosphatidylserine, a phospholipid that resides in the inner leaflet of the plasma membrane, is transiently exposed to cell surface and promotes myoblast fusion. We show that cell surface phosphatidylserine inhibits PIEZO1 and that the inward translocation of phosphatidylserine, which is driven by the phospholipid flippase complex of ATP11A and CDC50A, is required for PIEZO1 activation. PIEZO1-mediated Ca2+ influx promotes RhoA/ROCK-mediated actomyosin assemblies at the lateral cortex of myotubes, thus preventing uncontrolled fusion of myotubes and leading to polarized elongation during myotube formation. These results suggest that cell surface flip-flop of phosphatidylserine acts as a molecular switch for PIEZO1 activation that governs proper morphogenesis during myotube formation.
UR - https://www.scopus.com/pages/publications/85047608191
U2 - 10.1038/s41467-018-04436-w
DO - 10.1038/s41467-018-04436-w
M3 - Article
C2 - 29799007
AN - SCOPUS:85047608191
SN - 2041-1723
VL - 9
JO - Nature communications
JF - Nature communications
IS - 1
M1 - 2049
ER -