3' mRNA-seq analysis from murine satellite cells upon lnc-Rewind knockdown
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE141396 | GEO | 2021/01/12
REPOSITORIES: GEO
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Project description:3' mRNA-seq analysis from murine satellite cells upon lnc-Rewind knockdown
| PRJNA593267 | ENA
Project description:Satellite cells are resident skeletal muscle stem cells responsible for muscle maintenance and repair. In resting muscle, satellite cells are maintained in a quiescent state. Satellite cell activation induces the myogenic commitment factor, MyoD, and cell cycle entry to facilitate transition to a population of proliferating myoblasts that eventually exit the cycle and regenerate muscle tissue. The molecular mechanism involved in the transition of a quiescent satellite cell to a transit-amplifying myoblast is poorly understood. We used microarrays to detail the global program of gene expression of in vivo satellite cell activation through muscle injury and identified RNA post-transcriptional regulation as a key component of satellite cell activation. Wild type or Sdc4-/- satellite cells were FACS isolated from resting muscle or from muscle 12h and 48h following barium chloride-induced muscle injury. 5000 cell equivalents of RNA was labeled and hybridized to MOE430v2 GeneChips (Affymetrix) and scanned as per manufacturers protocol. Probeset intensities were GCRMA normalized for further analysis including UPGMA hierarchical clustering, analysis of variance (ANOVA), and fold change.
2012-07-31 | E-GEOD-38870 | biostudies-arrayexpress
Project description:Satellite cells are resident skeletal muscle stem cells responsible for muscle maintenance and repair. In resting muscle, satellite cells are maintained in a quiescent state. Satellite cell activation induces the myogenic commitment factor, MyoD, and cell cycle entry to facilitate transition to a population of proliferating myoblasts that eventually exit the cycle and regenerate muscle tissue. The molecular mechanism involved in the transition of a quiescent satellite cell to a transit-amplifying myoblast is poorly understood. We used microarrays to detail the global program of gene expression of in vivo satellite cell activation through muscle injury and identified RNA post-transcriptional regulation as a key component of satellite cell activation.
2012-08-01 | GSE38870 | GEO
Project description:The acquisition of a proliferating cell status from a quiescent state as well as the shift between proliferation and differentiation are key developmental steps in skeletal-muscle stem cells (satellite cells) to provide proper muscle regeneration. However, how satellite-cell proliferation is regulated, though, is not fully understood. Here, we report that the c-isoform of the transcription factor Pitx2 increases cell proliferation in myoblasts by down-regulating the miRNAs miR-15b, miR-23b, miR-106b, and miR-503. This Pitx2c-miRNA pathway also regulates cell proliferation in early-activated satellite cells, enhancing the Myf5+ satellite cells and thereby promoting their commitment to a myogenic cell fate. This study reveals unknown functions of several miRNAs in myoblast and satellite-cell behaviour and thus may have future applications in regenerative medicine. mirVana microarrays (Ambion) were used to profile microRNA signature at different Pitx2 overexpression conditions, namely two different doses (4 and 8 µg CMV-Pitx2c plasmid, respectively) after 24 hours of transfection in SOL8 skeletal myogenic cells. 20 µg of total RNA was used to hybridize two distinct microRNA microarrays on each condition analyzed.
2015-06-10 | E-GEOD-53943 | biostudies-arrayexpress
Project description:The acquisition of a proliferating cell status from a quiescent state as well as the shift between proliferation and differentiation are key developmental steps in skeletal-muscle stem cells (satellite cells) to provide proper muscle regeneration. However, how satellite-cell proliferation is regulated, though, is not fully understood. Here, we report that the c-isoform of the transcription factor Pitx2 increases cell proliferation in myoblasts by down-regulating the miRNAs miR-15b, miR-23b, miR-106b, and miR-503. This Pitx2c-miRNA pathway also regulates cell proliferation in early-activated satellite cells, enhancing the Myf5+ satellite cells and thereby promoting their commitment to a myogenic cell fate. This study reveals unknown functions of several miRNAs in myoblast and satellite-cell behaviour and thus may have future applications in regenerative medicine.
2015-06-10 | GSE53943 | GEO
Project description:Cytoplasmic long non coding RNAs have been shown to act at many different levels to control post-transcriptional gene expression; though their role in translational control is still poorly understood. Here we show that lnc-31 is a translational activator of Rock1, a negative regulator of myogenesis which prevents the exit of myoblasts from the cell cycle. This activity well correlates with the described role of lnc-31 in supporting myoblast proliferation. We show that lnc-31 binds the translational regulator YB-1 and targets the Rock1 mRNA by direct base pair interaction. We present evidences that lnc-31 stabilizes YB-1 on the Rock1 mRNA; this effect would in turn allow the YB-1-dependent remodelling of the Rock1 5’UTR and the promotion of its translation.
2018-05-09 | GSE102158 | GEO
Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.
2018-11-07 | PXD011577 | Pride
Project description:Satellite cells are myogenic precursor cells in adult skeletal muscle and play a crucial role in skeletal muscle repair, remodeling, and maintenance. Like myoblasts, satellite cells have the ability to proliferate, differentiate, and fuse to form multinucleated myofibers. In this study we aimed to identify the enhancers and the transcription factors binding to these enhancers that control gene expression in proliferating and differentiating bovine satellite cells. Using ChIP-seq, we identified 56,973 and 54,470 active enhancers, genomic regions marked with both H3K4me1 and H3K27ac, and 50,956 and 59,174 repressed enhancers, genomic regions marked with H3K27me3, in proliferating and differentiating bovine satellite cells, respectively. Motif enrichment analyses revealed many transcription factors including the AP-1 family transcription factors that regulate gene expression in proliferating bovine satellite cells and many transcription factors besides MyoG that regulate gene expression in differentiating bovine satellite cells.
2024-03-20 | GSE253395 | GEO
Project description:Hippo effectors Yap and Taz, Vgll1-4 and Tead 1-4 transcription factors have been linked to satellite cell/ myoblast proliferation and differentiation, muscle function and disease. The molecular function of Vgll3 in skeletal muscle stem cells was investigated using analysis of gene expression by microarrays to determine Vgll3 mediated gene expression changes and compare those to previously determined Taz and Yap mediated changes. Satellite cell-derived myoblasts were transduced with Vgll3 retrovirus for 24h or 48h, with empty retrovirus vector as control. Triplicate microarray analysis of empty vector controls and Vgll3 transgenic primary myoblasts were conducted.
2019-06-17 | E-MTAB-7614 | biostudies-arrayexpress
Project description:The regeneration of skeletal muscle relies on satellite cells which can proliferate, differentiate and form new myofibers upon injury. Emerging evidence suggests that misregulations of satellite cell fate and function influence the severity of Duchenne Muscular Dystrophy (DMD). The myogenic identity and maintenance of the pool of satellite cells is determined by the transcription factor PAX7. Satellite cell proliferation and self-renewal is regulated by the circadian clock. Here, we show that the CLOCK-interacting protein, Circadian (CIPC), a negative-feedback regulator of the circadian clock, is up-regulated during myoblast differentiation. Specific deletion of CIPC in satellite cells alleviated myopathy, improved muscle function and reduced fibrosis in mdx mice. CIPC deficiency led to activation of the ERK1/2 and JNK1/2 signaling pathways, which in turn activated the transcription factor SP1 to trigger the transcription of PAX7. Therefore, CIPC is a negative regulator of satellite cell function and loss of CIPC in satellite cells promotes muscle regeneration.
2022-01-27 | GSE195468 | GEO