Link to bioRxiv paper:
http://biorxiv.org/cgi/content/short/2022.11.02.514556v1?rss=1

Authors: Kneppers, A. E. M., Theret, M., Ben Larbi, S., Gsaier, L., Saugues, A., Dabadie, C., Ferry, A., Sakamoto, K., Mounier, R.

Abstract:
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 AMPK2 in the coordination of these events supporting myonuclear accretion. We demonstrate that AMPK2 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 AMPK2 in the regulation of myonuclear accretion, which is mediated by phosphorylation of the non-metabolic substrate BAIAP2. Similar cell tracing in vivo shows that AMPK2 knockout mice have a lower rate of myonuclear accretion during regeneration, and that MuSC-specific AMPK2 deletion decreases myonuclear accretion in response to myofiber contraction. Together, this demonstrates that AMPK2 is a MuSC-intrinsic regulator of myonuclear accretion.

Copy rights belong to original authors. Visit the link for more info

Podcast created by Paper Player, LLC