Journal
CELL DEATH AND DIFFERENTIATION
Volume 25, Issue 11, Pages 1921-1937Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41418-018-0165-9
Keywords
-
Categories
Funding
- National Research Foundation of Korea (NRF) - Korea government [NRF-2016R1D1A1B03933763, NRF-2011-0030072, NRF-2017R1A2B2007870, NRF-2018R1A6A1A03025124]
- MRC [MC_UU_00015/3] Funding Source: UKRI
Ask authors/readers for more resources
Muscle differentiation is a crucial process controlling muscle development and homeostasis. Mitochondrial reactive oxygen species (mtROS) rapidly increase and function as critical cell signaling intermediates during the muscle differentiation. However, it has not yet been elucidated how they control myogenic signaling. Autophagy, a lysosome-mediated degradation pathway, is importantly recognized as intracellular remodeling mechanism of cellular organelles during muscle differentiation. Here, we demonstrated that the mtROS stimulated phosphatidylinositol 3 kinase/AKT/mammalian target of rapamycin (mTOR) cascade, and the activated mTORC1 subsequently induced autophagic signaling via phosphorylation of uncoordinated-51-like kinase 1 (ULK1) at serine 317 and upregulation of Atg proteins to prompt muscle differentiation. Treatment with MitoQ or rapamycin impaired both phosphorylation of ULK1 and expression of Atg proteins. Therefore, we propose a novel regulatory paradigm in which mtROS are required to initiate autophagic reconstruction of cellular organization through mTOR activation in muscle differentiation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available