Expression data for C2C12 differentiation disrupted by Lrrfip1 knockdown
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE66924 | GEO | 2015/04/01
SECONDARY ACCESSION(S): PRJNA278371
REPOSITORIES: GEO
Similar Datasets
Project description:C2C12 myoblasts differentiation is a precise controlled process. Splicing of many genes changes during the differentiation process. Some muscle-specific splicing isoforms play important role in myogenesis. We used microarrays to detail the global programme of gene expression underlying defect of lrrfip1a, a muscle specific splicing isoform of Lrrfip1. Differentiated C2C12 myoblasts shLUCI or shLrrfip1a were collected and extracted RNA, then hybridizated on Affymetrix. We sought to obtain the different expressed genes between shLUCI and shLrrfip1a samples.
2015-04-01 | E-GEOD-66924 | biostudies-arrayexpress
Project description:C2C12 myoblast is a model that has been used extensively to study the process of skeletal muscle differentiation. Proteomics has advanced our understanding of skeletal muscle biology and the process of myogenesis. However, there is still no deep coverage of C2C12 myoblast proteome, which is important for the understanding of key drivers for the differentiation of skeletal muscle cells. Here, we conducted a multi-dimensional proteome profiling with TiSH strategy to get a comprehensive analysis of proteome, phosphoproteome and N-linked sialylated glycoproteome of C2C12 myoblasts. A total of 8313 protein groups were identified in C2C12 myoblasts, including 7827 protein groups from non-modified peptides, 3803 phosphoproteins and 977 formerly N-linked sialylated glycoproteins.
2020-11-27 | PXD011334 | Pride
Project description:Phosphoproteomic analysis of myogenesis in C2C12 myoblasts differentiating into myotubes. Four time points were analysed (0min, 30min, 24h and 5d) with four biological replicates.
2024-01-26 | PXD023413 | Pride
Project description:Tamoxifen, a selective estrogen receptor modulator (SERM), is commonly used in the treatment of hormone-responsive cancers. The effects of tamoxifen in anabolic tissues harboring estrogen-receptors, such as skeletal muscle, are poorly understood. As estrogen and estrogen receptors play an important role in skeletal muscle development and repair, we hypothesize that tamoxifen may have specific effects on myogenesis, the developmental process underlying muscle cells differentiation and repair. Myogenesis is characterized by fine-tuned changes in protein expression as embryonic myoblasts and adult satellite cells transition from pluripotent stem cells to multinucleated, contractile muscle fibers: we undertake a quantitative proteomic analysis of tamoxifen-induced changes in developing skeletal muscle cells which we expect may also shed light on the effect of tamoxifen on muscle repair.
We report a tandem mass-tag (TMT) approach to tamoxifen-treated myogenesis in C2C12 cells, a well-characterized model of in vitro murine skeletal muscle differentiation. A longitudinal analysis of >10,000 proteins identified in C2C12 myogenesis revealed a novel subset of 1,239 myogenically-regulated proteins. This set of regulatory proteins clustered into five distinct longitudinal expression trends which significantly overlap those obtained in similar analyses performed in human myocytes. A longitudinal analysis of myogenesis in the presence of tamoxifen, when contrasted with a similar analysis in untreated myogenesis finds that while the vast majority of myogenically-regulated proteins were unaffected by tamoxifen treatment, specific pathways and networks are affected. We document a specific functional enrichment for adiponectin-signaling, whereby a set of 198 proteins were differentially expressed relative to controls at one or more stages of myogenesis, the majority of which were involved in steroid biosynthesis, lipid storage and/or metal ion homeostasis. Interestingly, the only protein that was differentially expressed in the tamoxifen-treated cells at every stage of myogenesis was metallothionein-1 (MT1). Elevated levels of MT1 have been correlated with tamoxifen resistance and increased patient mortality and relapse in breast cancer, as well as with cachexia and muscle atrophy in rodent models. Increased MT1 expression levels may contribute to the musculoskeletal effects reported by patients undergoing tamoxifen treatment. Finally, we present a powerful, self-validating pipeline for analyzing the total proteomic response to in vitro treatment across every stage of muscle cells development which can be easily adapted to study the effects of other drugs on myogenesis.
2023-06-07 | MSV000092126 | MassIVE
Project description:C2C12 is a myoblast cell line usually used for study of muscle differentiation. Myod1 is a pro-differentiation factor for myogenesis. We found that CRISPR/Cas9-mediated Myod1 gene knockout in C2C12 cells led to the loss of myoblast identity and gain of neural properties.
2021-01-27 | GSE137507 | GEO
Project description:We report that differentiation of the C2C12 myoblast line on patterened hydrogels results in the increased expression of muscle sarcomere genes and more closely models expression changes that happen in in vivo muscle differentiation than do C2C12 myoblasts cultured on unpatterened substrates.
2020-04-15 | GSE148667 | GEO
Project description:Members of the SMYD family of Histone Lysine Methyltransferases, including SMYD3, were shown to be involved in both cardiac and skeletal myogenesis. Currently, very little is known about their mechanisms of action and their potential target genes. To study the cellular and molecular function of SMYD3 in skeletal muscle differentiation, we used loss and gain of function approaches in C2C12 myoblasts. We used RNA sequencing (RNA-seq) to generate gene expression profiling during myogenic differentiation under SMYD3 transient knockdown by siRNAs or SMYD3 stable overexpression in C2C12. We identified multiple genes whose expression is significantly affected by Smyd3 levels, among them the key myogenic regulatory factor (MRF) Myogenin.
2019-09-25 | GSE137954 | GEO
Project description:The Z-disc is a protein-rich structure critically important for myofibril development and integrity. In order to monitor the quantiative changes in C2C12 myoblast during myogenesis, a quantitative dimethyl-labelling approach was performed with d0 myoblasts, d5 myotubes and electrical puls stimulated d5 myotubes.
2017-01-02 | PXD004960 | Pride
Project description:Skeletal muscle differentiation (myogenesis) is a complex and highly coordinated biological process regulated by a series of myogenic marker genes. Chromatin interactions between gene’s promoters and their enhancers have an important role in transcriptional control. However, the high-resolution chromatin interactions of myogenic genes and their functional enhancers during myogenesis remain largely unclear. Here, we used circularized chromosome conformation capture coupled with next-generation sequencing (4C-seq) to investigate eight myogenic marker genes in C2C12 myoblasts (C2C12-MBs) and C2C12 myotubes (C2C12-MTs). We revealed dynamic chromatin interactions of these marker genes during differentiation, and identified 163 and 314 significant interaction sites (SISs) in C2C12-MBs and C2C12-MTs, respectively. The interacting genes of SISs in C2C12-MTs were mainly involved in muscle development, and histone modifications of the SISs changed during differentiation. Through functional genomic screening, we also identified 25 and 41 putative active enhancers in C2C12-MBs and C2C12-MTs, respectively. Using luciferase reporter assays for putative enhancers of Myog and Myh3, we identified eight activating enhancers. Furthermore, dCas9-KRAB epigenome editing and RNA-seq revealed a role for Myog enhancers in the regulation of Myog expression and myogenic differentiation in the native genomic context. Taken together, this study lays the groundwork for understanding 3D chromatin interaction changes of myogenic genes during myogenesis and provides insights that contribute to our understanding of the role of enhancers in regulating myogenesis.
2022-06-10 | GSE201138 | GEO
Project description:Background: Follistatin (FS) is an activin-binding glycoprotein, known for its antagonistic action on the TGF-β super-family of cytokines. It has ability to prevent muscle atrophy and to stimulate muscle growth through binding of myostatin (GDF8). FS does not cause these changes only by inhibition of GDF8 but this mechanism is still not well elucidated. In order to identify GDF8-dependent and GDF8-independent action of FS, we performed comprehensive transcriptomic analysis of differentiating C2C12 mouse myoblasts. Results: To evaluate influence of FS-288 (200ng/ml) on differentiating C2C12 myoblasts was used immunofluorescence analysis of MyHC protein expression in the culture and counting of the number and type of myotubes. Differentiating myoblasts treated with FS showed increase in number and size of myotubes. Microarray studies performed by us identified 30 genes oppositely regulated by FS and GDF8. Analyses of the transcriptomic profiles showed that FS has highly significant influence, associated with GDF8 binding, on the regulation of cell cycle, transport processes, cell communication, cell adhesion, cell motion, developmental processes and binding functions. The signalling pathways that may play a primary role in the myogenesis stimulation by FS are associated with TGF-β, Delta-Notch and Wnt signalling pathways, integrin and actin cytoskeleton signalling and adipogenesis regulation. Changes in expression of Hgf, Sort1, Trdn, Stmn2, Hdac1 genes, significantly involved in the process of myoblasts differentiation were validated with Real-Time PCR method. Conclusions: Our results implicate which aspects of transcriptional regulation of myogenesis process by FS could have significant and protective influence. We have shown that FS activity is associated not only with GDF8 binding but also with inhibited expression of genes involved in TGF-β signalling and by regulating of genes associated with vesicle transport apoptosis signalling pathway, inflammatory pathways and adipogenesis expression. Our analysis showed that follistatin GDF8-independent on differentiating myotubes involves regulation of localization processes, cell-matrix adhesion, mRNA processing, apoptosis, fatty acid metabolic processes, SNAP receptor activity functions and partial regulation of transcription processes. These results give a new and complete image of the follistatin role in the muscle cell differentiation and indicate target genes for FS which in the future may be a good therapeutic approach.
2014-10-31 | GSE59775 | GEO