scholarly journals Distinct metabolic states govern skeletal muscle stem cell fates during prenatal and postnatal myogenesis

2018 ◽  
Vol 131 (14) ◽  
pp. jcs212977 ◽  
Author(s):  
Francesca Pala ◽  
Daniela Di Girolamo ◽  
Sébastien Mella ◽  
Siham Yennek ◽  
Laurent Chatre ◽  
...  
2019 ◽  
Vol 33 (7) ◽  
pp. 8094-8109 ◽  
Author(s):  
Shimpei Hori ◽  
Yosuke Hiramuki ◽  
Daigo Nishimura ◽  
Fuminori Sato ◽  
Atsuko Sehara-Fujisawa

2009 ◽  
Vol 187 (7) ◽  
pp. 941-943 ◽  
Author(s):  
Andrew B. Lassar

In this issue, Gillespie et al. (Gillespie et al. 2009. J. Cell Biol. doi:10.1083/jcb.200907037) demonstrate that the mitogen-activated protein kinase isoform p38-γ plays a crucial role in blocking the premature differentiation of satellite cells, a skeletal muscle stem cell population. p38-γ puts the brakes on skeletal muscle differentiation by promoting the association of the transcription factor MyoD with the histone methyltransferase, KMT1A, which act together in a complex to repress the premature expression of the gene encoding the myogenic transcription factor Myogenin.


2013 ◽  
Vol 144 (5) ◽  
pp. S-886
Author(s):  
Johanna G. Palmadottir ◽  
Francisco A. Sylvester ◽  
Morgan E. Carlson ◽  
Andrew Draghi

2011 ◽  
Vol 15 (10) ◽  
pp. 2269-2272 ◽  
Author(s):  
Florina M. Bojin ◽  
Oana I. Gavriliuc ◽  
Mirabela I. Cristea ◽  
Gabriela Tanasie ◽  
Carmen S. Tatu ◽  
...  

2019 ◽  
Author(s):  
Bradley Pawlikowski ◽  
Nicole Dalla Betta ◽  
Tiffany Antwine ◽  
Bradley B. Olwin

SummarySkeletal muscle maintenance and repair is dependent on the resident adult muscle stem cell (MuSC). During injury, and in diseased muscle, stem cells are engaged to replace or repair damaged muscle, which requires the stem cells to exit quiescence and expand, followed by differentiation to regenerate myofibers and self-renewal to replenish the stem cell population. Following an injury, little is known regarding the timing of MuSC (skeletal muscle stem cell) self-renewal, myoblast expansion or myoblast differentiation. To determine the timing and kinetics of these cell fate decisions, we employed DNA-based lineage tracing to label newly replicated cells and followed cell fates during skeletal muscle regeneration. MuSCs activate and expand as myoblasts rapidly following injury, where the majority differentiate into myonuclei, establishing the centrally located myonuclear pool. Re-establishing the majority MuSC pool by self-renewal occurs after 5 days post-muscle injury, accompanied by low levels of myonuclear accretion that generate only peripheral myonuclei. In aged mice, possessing ∼1/2 the number of MuSCs present in young adult mice, the timing of post injury MuSC self-renewal is delayed, and although MuSCs expansion as myoblasts in aged muscle is impaired, the number of MuSC unexpectedly recovers to young adult levels during regeneration. Following an induced muscle injury, we found that myonuclei are generated within the first four days post injury derived from myoblasts expanding from activated MuSCs. Only later during regeneration, from 5 d to 14 d post injury, is the MuSC pool replenished by self-renewal, accompanied by generation of peripheral myonuclei.


2021 ◽  
Vol 1 (10) ◽  
Author(s):  
Svenja C. Schüler ◽  
Simon Dumontier ◽  
Jonathan Rigaux ◽  
C. Florian Bentzinger

2015 ◽  
Vol 7 (2) ◽  
pp. 73
Author(s):  
Anna Meiliana ◽  
Nurrani Mustika Dewi ◽  
Andi Wijaya

BACKGROUND: Age-related muscle loss leads to lack of muscle strength, resulting in reduced posture and mobility and an increased risk of falls, all of which contribute to a decrease in quality of life. Skeletal muscle regeneration is a complex process, which is not yet completely understood.CONTENT: Skeletal muscle undergoes a progressive age-related loss in mass and function. Preservation of muscle mass depends in part on satellite cells, the resident stem cells of skeletal muscle. Reduced satellite cell function may contribute to the age-associated decrease in muscle mass. Recent studies have delineated that the aging process in organ stem cells is largely caused by age-specific changes in the differentiated niches, and that regenerative outcomes often depend on the age of the niche, rather than on stem cell age. It is likely that epigenetic states will be better define such key satellite cell features as prolonged quiescence and lineage fidelity. It is also likely that DNA and histone modifications will underlie many of the changes in aged satellite cells that account for age-related declines in functionality and rejuvenation through exposure to the systemic environment.SUMMARY: Skeletal muscle aging results in a gradual loss of skeletal muscle mass, skeletal muscle function and regenerative capacity, which can lead to sarcopenia and increased mortality. Although the mechanisms underlying sarcopenia remain unclear, the skeletal muscle stem cell, or satellite cell, is required for muscle regeneration. Decreased muscle stem cell function in aging has long been shown to depend on altered environmental cues, whereas the contribution of intrinsic mechanisms remained less clear. Signals in the aged niche were shown to cause permanent defects in the ability of satellite cells to return to quiescence, ultimately also impairing the maintenance of self-renewing satellite cells. Therefore, only anti-aging strategies taking both factors, the stem cell niche and the stem cells per se, into consideration may ultimately be successful.KEYWORDS: satellite cell, muscle, aging, niche, regenerations


2021 ◽  
Author(s):  
Huating WANG ◽  
Yu Zhao ◽  
Yingzhe Ding ◽  
Liangqiang He ◽  
Yuying Li ◽  
...  

Abstract 3D genome rewiring is known to influence spatiotemporal expression of lineage-specific genes and cell fate transition during stem cell differentiation and aging processes. Yet it is unknown how 3D architecture remodels and orchestrates transcriptional changes during skeletal muscle stem cell (also called satellite cell, SC) activation, proliferation and differentiation course. Here, using in situ Hi-C we comprehensively map the 3D genome topology reorganization at multiscale levels during mouse SC lineage progression and integrate with transcriptional and chromatin signatures to elucidate how 3D genome rewiring dictates gene expression program. Specifically, rewiring at compartment level is most pronounced when SC becomes activated. Striking loss in TAD border insulation and chromatin looping also occurs during early activation process. Meanwhile, TADs can also form TAD clusters and super-enhancer containing TAD clusters orchestrate stage-specific gene expression during SC early activation. Furthermore, we elucidate 3D chromatin regulation of key transcription factor, PAX7 and identify cis-regulatory elements that are crucial for local chromatin architecture and Pax7 expression. Lastly, 3D genome remodeling is profiled in SCs isolated from naturally aging mice, unveiling that geriatric SCs display a prominent gain in long-range contacts and loss of TAD border insulation. Genome compartmentalization and chromatin looping are evidently altered in aged SC while geriatric SC display a more prominent loss in strength of TAD borders. Together, our results implicate 3D chromatin extensively reorganizes at multiple architectural levels and underpin the transcriptome remodeling during SC lineage development and SC aging.


2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Alec Marc Dupont ◽  
Davis Englund ◽  
John McCarthy ◽  
Charlotte Peterson

Cell Reports ◽  
2020 ◽  
Vol 30 (10) ◽  
pp. 3583-3595.e5 ◽  
Author(s):  
Andrea J. De Micheli ◽  
Emily J. Laurilliard ◽  
Charles L. Heinke ◽  
Hiranmayi Ravichandran ◽  
Paula Fraczek ◽  
...  

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