CCAAT/enhancer-binding protein beta promotes muscle stem cell quiescence through regulation of quiescence-associated genes

Stem Cells ◽  
2020 ◽  
Vol 39 (3) ◽  
pp. 345-357
Author(s):  
Neena Lala-Tabbert ◽  
Hamood AlSudais ◽  
François Marchildon ◽  
Dechen Fu ◽  
Nadine Wiper-Bergeron
Keyword(s):  
Stem Cell ◽  
Binding Protein ◽  
Muscle Stem Cell ◽  
Stem Cell Quiescence ◽  
Enhancer Binding Protein ◽  
Cell Quiescence ◽  
Ccaat Enhancer Binding Protein

scholarly journals Phosphorylation of eIF2α Is a Translational Control Mechanism Regulating Muscle Stem Cell Quiescence and Self-Renewal

2016 ◽  
Vol 18 (1) ◽  
pp. 79-90 ◽  
Author(s):  
Victoria Zismanov ◽  
Victor Chichkov ◽  
Veronica Colangelo ◽  
Solène Jamet ◽  
Shuo Wang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Translational Control ◽  
Control Mechanism ◽  
Self Renewal ◽  
Muscle Stem Cell ◽  
Stem Cell Quiescence ◽  
Cell Quiescence

scholarly journals Induction of muscle stem cell quiescence by the secreted niche factor Oncostatin M

2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Srinath C. Sampath ◽  
Srihari C. Sampath ◽  
Andrew T. V. Ho ◽  
Stéphane Y. Corbel ◽  
Joshua D. Millstone ◽  
...  
Keyword(s):  
Stem Cell ◽  
Oncostatin M ◽  
Muscle Stem Cell ◽  
Stem Cell Quiescence ◽  
Cell Quiescence ◽  
Niche Factor

scholarly journals Induction of muscle stem cell quiescence by the secreted niche factor Oncostatin M

2018 ◽  
Author(s):  
Srinath C. Sampath ◽  
Srihari C. Sampath ◽  
Andrew T.V. Ho ◽  
Stéphane Y. Corbel ◽  
Joshua D. Millstone ◽  
...  
Keyword(s):  
Stem Cell ◽  
Oncostatin M ◽  
Solid Organ ◽  
Muscle Stem Cell ◽  
Potent Inducer ◽  
Disease States ◽  
Stem Cell Quiescence ◽  
Cell Quiescence ◽  
Niche Factor

AbstractThe balance between stem cell quiescence and proliferation in skeletal muscle is tightly controlled, but perturbed in a variety of disease states. Despite progress in identifying activators of stem cell proliferation, the niche factor(s) responsible for quiescence induction remain unclear. Here we report an in vivo imaging-based screen which identifies Oncostatin M (OSM), a member of the interleukin-6 family of cytokines, as a potent inducer of muscle stem cell (MuSC, satellite cell) quiescence. OSM is produced by muscle fibers, induces reversible MuSC cell cycle exit, and maintains stem cell regenerative capacity as judged by serial transplantation. Conditional OSM receptor deletion in satellite cells leads to stem cell depletion and impaired regeneration following injury. These results identify Oncostatin M as a secreted niche factor responsible for quiescence induction, and for the first time establish a direct connection between induction of quiescence, stemness, and transplantation potential in solid organ stem cells.

scholarly journals mRNP Granule Proteins Fmrp and Dcp1a Differentially Regulate Muscle Stem Cell Quiescence via Reciprocally Regulating mRNP Complexes

2020 ◽  
Author(s):  
Nainita Roy ◽  
Malini Pillai ◽  
Farah Patell-Socha ◽  
Swetha Sundar ◽  
Sravya Ganesh ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Sectional Area ◽  
Cross Sectional ◽  
Muscle Stem Cell ◽  
Translational Repressor ◽  
Stem Cell Quiescence ◽  
Cell Quiescence ◽  
Granule Proteins

Abstract Background: During skeletal muscle regeneration, satellite stem cells use distinct pathways to repair damaged myofibers or to self-renew by returning to quiescence. Cellular/mitotic quiescence employs mechanisms that promote a poised or primed state, including altered RNA turnover and translational repression. Here, we investigate the role of mRNP granule proteins Fragile X Mental Retardation Protein (Fmrp) and Decapping protein 1a (Dcp1a) in muscle stem cell quiescence and differentiation.Methods: Using isolated single muscle fibers from adult mice, we established differential enrichment of mRNP granule proteins including Fmrp and Dcp1a in muscle stem cells vs. myofibers. We investigated muscle tissue homeostasis in adult Fmr1-/- mice, analyzing myofiber cross-sectional area in vivo and satellite cell proliferation ex vivo. We explored the molecular mechanisms of Dcp1a and Fmrp function in quiescence, proliferation and differentiation in a C2C12 culture model. Here, we used polysome profiling, imaging and RNA/protein expression analysis to establish the abundance and assembly status of mRNP granule proteins in different cellular states, and the phenotype of knockdown cells.Results: Quiescent muscle satellite cells are enriched for puncta containing the translational repressor Fmrp, but not the mRNA decay factor Dcp1a. MuSC isolated from Fmr1-/- mice exhibit defective proliferation and mature myofibers show reduced cross-sectional area, suggesting a role for Fmrp in muscle homeostasis. Expression and organization of Fmrp and Dcp1a varies between different cell states in culture. Consistent with its role as a translational repressor, Fmrp is enriched in non-translating mRNP complexes abundant in quiescent myoblasts; Dcp1a puncta are lost in quiescence, suggesting stabilized and repressed transcripts. The function of each protein differs during proliferation; whereas Fmrp knockdown led to decreased proliferation and lower cyclin expression, Dcp1a knockdown led to increased cell proliferation and higher cyclin expression. However, knockdown of either Fmrp or Dcp1a led to compromised differentiation. We also observed cross-regulation of decay versus storage mRNP granules; knockdown of Fmrp enhances accumulation of Dcp1a puncta, whereas knockdown of Dcp1a leads to increased Fmrp in puncta.Conclusions: Taken together, our results provide evidence that the balance of mRNA turnover versus utilization is specific for distinct cellular states.

Sign in / Sign up

Export Citation Format

Share Document