AMPKα2 is a skeletal muscle stem cell intrinsic regulator of myonuclear accretion
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AMPKα2 is a skeletal muscle stem cell intrinsic regulator of myonuclear accretion. / Kneppers, Anita; Ben Larbi, Sabrina; Theret, Marine; Saugues, Audrey; Dabadie, Carole; Gsaier, Linda; Ferry, Arnaud; Rhein, Philipp; Gondin, Julien; Sakamoto, Kei; Mounier, Rémi.
In: iScience, Vol. 26, No. 12, 108343, 2023.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - AMPKα2 is a skeletal muscle stem cell intrinsic regulator of myonuclear accretion
AU - Kneppers, Anita
AU - Ben Larbi, Sabrina
AU - Theret, Marine
AU - Saugues, Audrey
AU - Dabadie, Carole
AU - Gsaier, Linda
AU - Ferry, Arnaud
AU - Rhein, Philipp
AU - Gondin, Julien
AU - Sakamoto, Kei
AU - Mounier, Rémi
N1 - Publisher Copyright: © 2023
PY - 2023
Y1 - 2023
N2 - Due to the post-mitotic nature of skeletal muscle fibers, adult muscle maintenance relies on dedicated muscle stem cells (MuSCs). In most physiological contexts, MuSCs support myofiber homeostasis by contributing to myonuclear accretion, which requires a coordination of cell-type specific events between the myofiber and MuSCs. Here, we addressed the role of the kinase AMPKα2 in the coordination of these events supporting myonuclear accretion. We demonstrate that AMPKα2 deletion impairs skeletal muscle regeneration. Through in vitro assessments of MuSC myogenic fate and EdU-based cell tracing, we reveal a MuSC-specific role of AMPKα2 in the regulation of myonuclear accretion, which is mediated by phosphorylation of the non-metabolic substrate BAIAP2. Similar cell tracing in vivo shows that AMPKα2 knockout mice have a lower rate of myonuclear accretion during regeneration, and that MuSC-specific AMPKα2 deletion decreases myonuclear accretion in response to myofiber contraction. Together, this demonstrates that AMPKα2 is a MuSC-intrinsic regulator of myonuclear accretion.
AB - Due to the post-mitotic nature of skeletal muscle fibers, adult muscle maintenance relies on dedicated muscle stem cells (MuSCs). In most physiological contexts, MuSCs support myofiber homeostasis by contributing to myonuclear accretion, which requires a coordination of cell-type specific events between the myofiber and MuSCs. Here, we addressed the role of the kinase AMPKα2 in the coordination of these events supporting myonuclear accretion. We demonstrate that AMPKα2 deletion impairs skeletal muscle regeneration. Through in vitro assessments of MuSC myogenic fate and EdU-based cell tracing, we reveal a MuSC-specific role of AMPKα2 in the regulation of myonuclear accretion, which is mediated by phosphorylation of the non-metabolic substrate BAIAP2. Similar cell tracing in vivo shows that AMPKα2 knockout mice have a lower rate of myonuclear accretion during regeneration, and that MuSC-specific AMPKα2 deletion decreases myonuclear accretion in response to myofiber contraction. Together, this demonstrates that AMPKα2 is a MuSC-intrinsic regulator of myonuclear accretion.
KW - cell Biology
KW - Molecular biology experimental approach
KW - Molecular mechanism of behavior
KW - Specialized functions of cells
KW - Stem cells research
U2 - 10.1016/j.isci.2023.108343
DO - 10.1016/j.isci.2023.108343
M3 - Journal article
C2 - 38077152
AN - SCOPUS:85179721274
VL - 26
JO - iScience
JF - iScience
SN - 2589-0042
IS - 12
M1 - 108343
ER -
ID: 378328325