Skeletal muscle maintenance and repair involve several finely coordinated steps in which pluripotent stem cells are activated, proliferate, exit the cell cycle and differentiate. This process is accompanied by activation of hundreds of muscle-specific genes and repression of genes associated with cell proliferation or pluripotency. Mechanisms controlling myogenesis are precisely coordinated and regulated in time to allow the sequence of activation/inactivation of genes expression. Muscular differentiation is the result of the interplay between several processes such as transcriptional induction, transcriptional repression and mRNA stability. mRNA stability is now recognized as an essential mechanism of control of gene expression. For instance, we previously showed that the endoribonuclease L (RNase L) and its inhibitor (RLI) regulates MyoD mRNA stability and consequently muscle differentiation

Bisbal, Catherine

Cambier, Linda

Manchon, Laurent

Regnier, Laëtitia

Salehzada, Tamim

Vu Thi, Nga

English

PubMed

Skeletal muscle maintenance and repair involve several finely coordinated steps in which pluripotent stem cells are activated, proliferate, exit the cell cycle and differentiate. This process is accompanied by activation of hundreds of muscle-specific genes and repression of genes associated with cell proliferation or pluripotency. Mechanisms controlling myogenesis are precisely coordinated and regulated in time to allow the sequence of activation/inactivation of genes expression. Muscular differentiation is the result of the interplay between several processes such as transcriptional induction, transcriptional repression and mRNA stability. mRNA stability is now recognized as an essential mechanism of control of gene expression. For instance, we previously showed that the endoribonuclease L (RNase L) and its inhibitor (RLI) regulates MyoD mRNA stability and consequently muscle differentiation.We now performed global gene expression analysis by SAGE to identify genes that were down-regulated upon activation of RNase L in C2C12 myogenic cells, a model of satellite cells. We found that RNase L regulates mRNA stability of factors implicated in the control of pluripotency and cell differentiation. Moreover, inappropriate RNase L expression in C2C12 cells led to inhibition of myogenesis and differentiation into adipocytes even when cells were grown in conditions permissive for muscle differentiation. Conversely, over-expression of RLI allowed muscle differentiation of myogenic C2C12 cells even in non permissive conditions.These findings reveal the central role of RNase L and RLI in controlling gene expression and cell fate during myogenesis. Our data should provide valuable insights into the mechanisms that control muscle stem cell differentiation and into the mechanism of metaplasia observed in aging or muscular dystrophy where adipose infiltration of muscle occurs

Tamim Salehzada

Linda Cambier

Nga Vu Thi

Laurent Manchon

Laëtitia Regnier

Catherine Bisbal

Directory of Open Access Journals

PLoS ONE

Endoribonuclease L (RNase L) regulates the myogenic and adipogenic potential of myogenic cells.

International audienceSkeletal muscle maintenance and repair involve several finely coordinated steps in which pluripotent stem cells are activated, proliferate, exit the cell cycle and differentiate. This process is accompanied by activation of hundreds of muscle-specific genes and repression of genes associated with cell proliferation or pluripotency. Mechanisms controlling myogenesis are precisely coordinated and regulated in time to allow the sequence of activation/inactivation of genes expression. Muscular differentiation is the result of the interplay between several processes such as transcriptional induction, transcriptional repression and mRNA stability. mRNA stability is now recognized as an essential mechanism of control of gene expression. For instance, we previously showed that the endoribonuclease L (RNase L) and its inhibitor (RLI) regulates MyoD mRNA stability and consequently muscle differentiation.We now performed global gene expression analysis by SAGE to identify genes that were down-regulated upon activation of RNase L in C2C12 myogenic cells, a model of satellite cells. We found that RNase L regulates mRNA stability of factors implicated in the control of pluripotency and cell differentiation. Moreover, inappropriate RNase L expression in C2C12 cells led to inhibition of myogenesis and differentiation into adipocytes even when cells were grown in conditions permissive for muscle differentiation. Conversely, over-expression of RLI allowed muscle differentiation of myogenic C2C12 cells even in non permissive conditions.These findings reveal the central role of RNase L and RLI in controlling gene expression and cell fate during myogenesis. Our data should provide valuable insights into the mechanisms that control muscle stem cell differentiation and into the mechanism of metaplasia observed in aging or muscular dystrophy where adipose infiltration of muscle occur

HAL Descartes

Endoribonuclease L (RNase L) Regulates the Myogenic and Adipogenic Potential of Myogenic Cells

Salehzada Tamim

Cambier Linda

Vu Thi Nga

Manchon Laurent

Regnier Laëtitia

Bisbal Catherine

Public Library of Science (PLOS)

59-modified agonist and antagonist (29-59)(A)n analogues: synthesis and biological activity.

A eukaryotic transcriptional repressor with carboxypeptidase activity.

A metaanalysis of human embryonic stem cells transcriptome integrated into a webbased expression atlas.

A myogenic cell line with altered serum requirements for differentiation.

A newly discovered function for RNase L in regulating translation termination.

A transcriptional signaling pathway in the IFN system mediated by 29-59-oligoadenylate activation of RNase L.

Activation of an adipogenic program in adult myoblasts with age.

Activation of the interferon system during myogenesis in vitro.

Adipogenic potential of human adipose derived stromal cells from multiple donors is heterogeneous.

Affinity labelling and characterization of the ppp(A29p)nA-dependent endoribonuclease from different mammalian sources.

An absolute method for protein determination based on difference in absorbance at 235 and 280 nm.

CCAAT/ Enhancer-binding protein homologous protein (CHOP) decreases bone formation and causes osteopenia.

Chromatin signature reveals over a thousand highly conserved large non-coding RNAs in mammals.

Cleavage of structural proteins during the assembly of the head of bacteriophage T4.

Cloning and characterization of a RNAse L inhibitor. A new component of the interferonregulated 2-5A pathway.

Compositional analysis of muscle in boys with Duchenne muscular dystrophy using MR imaging.

Congenital muscular dystrophy: Clinical and pathologic study of 50 patients with the classical (Occidental) merosin-positive form.

Control of muscle development by dueling HATs and HDACs.

Cytokines and chemokines are both expressed by human myoblasts: possible relevance for the immune pathogenesis of muscle inflammation.

Direct isolation of satellite cells for skeletal muscle regeneration.

Diverse functions of RNase L and implications in pathology.

Diversity of septin scaffolds.

Effect of serum on the down-regulation of CHOP-10 during differentiation of 3T3-L1 preadipocytes.

Endogenous interferongamma is required for efficient skeletal muscle regeneration.

Expression of a PKR dominant-negative mutant in myogenic cells interferes with the myogenic process.

Expression of ril, a novel LIM domain gene, is down-regulated in Hras-transformed cells and restored in phenotypic revertants.

Expression of specific white adipose tissue genes in denervation-induced skeletal muscle fatty degeneration.

Expression of the differentiation-induced gene for fatty acid-binding protein is activated by glucocorticoid and cAMP.

Genetic ablation of zyxin causes Mena/VASP mislocalization, increased motility, and deficits in actin remodeling.

H19 gene expression is up-regulated exclusively by stabilisation of the RNA during muscle cell differentiation.

HPC1/ RNASEL mediates apoptosis of prostate cancer cells treated with 29,59-oligoadenylates, topoisomerase I inhibitors, and tumor necrosis factor-related apoptosis-inducing ligand.

Identification of a common nucleotide sequence in the 39-untranslated region of mRNA molecules specifying inflammatory mediators.

Induction of the interferon-inducible RNA-degrading enzyme, RNase L, by stress-inducing agents in the human cervical carcinoma cells.

Infection with Moloney murine sarcoma virus inhibits myogenesis and alters the myogenic-associated (29-59)oligoadenylate synthetase expression and activity.

Insights into the molecular evolution of the PDZ/LIM family and identification of a novel conserved protein motif.

Interferon action: RNA cleavage pattern of a (29-59)oligoadenylate– dependent endonuclease.

Interruption of myogenesis by transforming growth factor beta 1 or EGTA inhibits expression and activity of the myogenic-associated (29-59) oligoadenylate synthetase and PKR [published erratum appears in Exp Cell Res

Involvement of PKR in the regulation of myogenesis.

JAK1-STAT1-STAT3, a key pathway promoting proliferation and preventing premature differentiation of myoblasts.

JAK2/STAT2/STAT3 Are Required for Myogenic Differentiation.

Muscle satellite cells are multipotential stem cells that exhibit myogenic, osteogenic, and adipogenic differentiation.

Muscle structural changes in mitochondrial myopathy relate to genotype.

Myoblasts and macrophages share molecular components that contribute to cell-cell fusion.

Myogenesis and the intermediate filament protein, nestin.

Nischarin, a novel protein that interacts with the integrin alpha5 subunit and inhibits cell migration.

Obesity and insulin resistance.

PKR is a novel functional direct player that coordinates skeletal muscle differentiation via p38MAPK/AKT pathways.

Post-transcriptional control of the interferon system. Biochimie 89: 761–769. RNase

Regulation of adipogenesis by a transcriptional repressor that modulates MAPK activation.

Regulation of mitochondrial mRNA stability by RNase L is translation-dependent and controls IFNalphainduced apoptosis.

Ribosomal RNA cleavage, nuclease activation and 2-5A(ppp(A29p)nA) in interferon-treated cells.

Role for stress fiber contraction in surface tension development and stretch-activated channel regulation in C2C12 myoblasts.

Role of C/EBP homologous protein (CHOP-10) in the programmed activation of CCAAT/enhancer-binding protein-beta during adipogenesis.

Role of the CCAAT enhancer binding proteins (C/EBPs) in adipocyte differentiation.

Roles of peroxisome proliferator-activated receptors delta and gamma in myoblast transdifferentiation.

Satellite-cell pool size does matter: defining the myogenic potency of aging skeletal muscle.

Serial analysis of gene expression [see comments].

Signaling chromatin to make muscle.

Sphingosine 1-phosphate induces cytoskeletal reorganization in C2C12 myoblasts: physiological relevance for stress fibres in the modulation of ion current through stretch-activated channels.

STAT3 and Oct-3/4 control histone modification through induction of Eed in embryonic stem cells.

Stem cell function, self-renewal, and behavioral heterogeneity of cells from the adult muscle satellite cell niche.

Stimulation of adipogenesis in fibroblasts by PPAR gamma 2, a lipid-activated transcription factor.

Sublines of mouse 3T3 cells that accumulate lipids.

Systemic inflammation and skeletal muscle dysfunction in chronic obstructive pulmonary disease: state of the art and novel insights in regulation of muscle plasticity.

Targeted inactivation of myogenic factor genes reveals their role during mouse myogenesis: a review.

The 29-59 oligoadenylate/RNase L/RNase L inhibitor pathway regulates both MyoD mRNA stability and muscle cell differentiation.

The emerging biology of satellite cells and their therapeutic potential.

The H19 gene: regulation and function of a non-coding RNA.

The human 29-59oligoadenylate synthetase family: unique interferon-inducible enzymes catalyzing 29-59 instead of 39-59 phosphodiester bond formation.

The increase in levels of interferon-inducible proteins p202a and p202b and RNA-dependent protein kinase (PKR) during myoblast differentiation is due to transactivation by MyoD: their tissue distribution in uninfected mice does not depend on interferons.

The nonamer UUAUUUAUU is the key AU-rich sequence motif that mediates mRNA degradation.

The PDZ-LIM protein RIL modulates actin stress fiber turnover and enhances the association of alpha-actinin with F-actin. Exp Cell Res 293: 117–128. RNase L Regulates Stem Cells

The role of 29-59 oligoadenylate-activated ribonuclease L in apoptosis.

The Skeletal Muscle Satellite Cell: The Stem Cell That Came In From the Cold.

The stability of mRNA influences the temporal order of the induction of genes encoding inflammatory molecules.

The synthesis and distribution of desmin and vimentin during myogenesis in vitro.

The WNT receptor FZD7 contributes to self-renewal signaling of human embryonic stem cells.

Thiazolidinediones and fatty acids convert myogenic cells into adipose-like cells.

Transcriptome analysis of monocytic leukemia cell differentiation.

Transdifferentiation of myoblasts by the adipogenic transcription factors PPAR gamma and C/EBP alpha.

Upregulation of gene encoding adipogenic transcriptional factors C/EBPalpha and PPARgamma2 in denervated muscle.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2762314

Endoribonuclease L (RNase L) Regulates the Myogenic and Adipogenic Potential of Myogenic Cells

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