Gene expression during chicken myogenesis
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ABSTRACT:
ORGANISM(S): Gallus gallus
PROVIDER: GSE148017 | GEO | 2020/04/03
REPOSITORIES: GEO
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Project description:Chick is an ideal model system for myogenesis study. Lots of genes would change their expression during myogenesis, however, is there any difference about gene expression between chick and mice? Our study represents the first detailed analysis of the transcriptomes of chicken primary myoblasts and myotubes, with biologic replicates, generated by RNA-seq technology. The data reported here may provide an important understanding of the genes involved in the regulation of chicken myogenesis.
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Project description:Chick is an ideal model system for myogenesis study. Lots of genes would change their expression during myogenesis, however, is there any difference about gene expression between chick and mice? Our study represents the first detailed analysis of the transcriptomes of chicken primary myoblasts and myotubes, with biologic replicates, generated by RNA-seq technology. The data reported here may provide an important understanding of the genes involved in the regulation of chicken myogenesis.
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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.
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Project description:Gene expression during chicken myogenesis
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Project description:Skeletal muscle contains long multinucleated and contractile structures known as muscle fibers, which arise from the fusion of myoblasts into nucleated myotubes during myogenesis. The myogenic regulatory factor (MRF) MYF5 is the earliest to be expressed during myogenesis and functions as a transcription factor in muscle progenitor cells (satellite cells) and myocytes. In mouse C2C12 myocytes, MYF5 is implicated in the initial steps of myoblast differentiation into myotubes. Ribonucleoprotein immunoprecipitation (RIP) analysis showed that MYF5 bound a subset of myoblast mRNAs; prominent among them was Ccnd1 mRNA, which encodes the key cell cycle regulator CCND1 (Cyclin D1). Biotin-RNA pulldown, UV-crosslinking, and gel shift experiments indicated that MYF5 was capable of binding the 3' untranslated region (UTR) and the coding region (CR) of Ccnd1 mRNA. MYF5 silencing in proliferating growing myoblasts revealed that and MYF5 promoted CCND1 translation, and it also modestly increased transcription of Ccnd1 mRNA. Importantly, silencing MYF5 reduced myoblast growth as well as differentiation of myoblasts into myotubes, while overexpressing MYF5 in C2C12 cells upregulated CCND1 expression. We propose that MYF5 enhances early myogenesis in part by coordinately elevating Ccnd1 transcription and Ccnd1 mRNA translation. Four replicates were utilized from either Control (IgG) or MYF5-immunoprecipitated RNA samples from C2C12 cells growing in either growth medium (GM) or differentiation medium (DM) for a total of sixteen samples.
2016-08-08 | E-GEOD-73704 | biostudies-arrayexpress
Project description:Skeletal muscle contains long multinucleated and contractile structures known as muscle fibers, which arise from the fusion of myoblasts into nucleated myotubes during myogenesis. The myogenic regulatory factor (MRF) MYF5 is the earliest to be expressed during myogenesis and functions as a transcription factor in muscle progenitor cells (satellite cells) and myocytes. In mouse C2C12 myocytes, MYF5 is implicated in the initial steps of myoblast differentiation into myotubes. Ribonucleoprotein immunoprecipitation (RIP) analysis showed that MYF5 bound a subset of myoblast mRNAs; prominent among them was Ccnd1 mRNA, which encodes the key cell cycle regulator CCND1 (Cyclin D1). Biotin-RNA pulldown, UV-crosslinking, and gel shift experiments indicated that MYF5 was capable of binding the 3' untranslated region (UTR) and the coding region (CR) of Ccnd1 mRNA. MYF5 silencing in proliferating growing myoblasts revealed that and MYF5 promoted CCND1 translation, and it also modestly increased transcription of Ccnd1 mRNA. Importantly, silencing MYF5 reduced myoblast growth as well as differentiation of myoblasts into myotubes, while overexpressing MYF5 in C2C12 cells upregulated CCND1 expression. We propose that MYF5 enhances early myogenesis in part by coordinately elevating Ccnd1 transcription and Ccnd1 mRNA translation.
2016-08-08 | GSE73704 | GEO
Project description:Myogenesis is a tightly controlled process involving the transcriptional activation and repression of thousands of genes. Although many components of the transcriptional network are known for the later phases of myogenesis, relatively little work has described the transcriptional landscape within the first 24 hours, when myoblasts commit to differentiate. Through dense temporal sampling of differentiating C2C12 myoblasts, we identify 266 transcriptional regulators (TRs) whose expression is altered within the first 12 hours of myogenesis. A high-content shRNA screen of 76 TRs involving 427 stable lines identified 48 genes whose knockdown significantly inhibits differentiation of C2C12 myoblasts. These include known regulators of myogenesis (Myod1, Myog and Myf5), as well as 26 regulators not previously associated with the process. Of the TRs differentially expressed within the first 24 hours, two-thirds inhibited differentiation when knocked down. Surprisingly, a similar proportion (67%) of shRNAs targeting TRs whose expression did not change during differentiation also inhibited myogenesis, suggesting that both stably and differentially expressed TRs are essential for this complex differentiation program. This implies that microarray-based approaches that concentrate functional validation studies on differentially-expressed genes will fail to identify many genes that are critically implicated in complex biological processes. C2C12 myoblasts were differentiated into myotubes and sampled at various timepoints for gene expression measurement on Illumina Mouse WG-6v1.1 arrays. Cells grown in separate plates were harvested at 12 different timepoints: t_0h, t_1h, t_1.5h, t_2h, t_3h, t_6h, t_9h, t_12h, t_24h, t_48h, t_96h, t_144h. All harvests were performed in triplicate using growths from successive passages.
2012-03-21 | E-GEOD-17038 | biostudies-arrayexpress
Project description:Analysis of Early Myogenesis Reveals an Extensive Set of Transcriptional Regulators Whose Knock-down Can Inhibit Differentiation Myogenesis is a tightly controlled process involving the transcriptional activation and repression of thousands of genes. Although many components of the transcriptional network are known for the later phases of myogenesis, relatively little work has described the transcriptional landscape within the first 24 hours, when myoblasts commit to differentiate. Through dense temporal sampling of differentiating C2C12 myoblasts, we identify 266 transcriptional regulators (TRs) whose expression is altered within the first 12 hours of myogenesis. A high-content shRNA screen of 76 TRs involving 427 stable lines identified 48 genes whose knockdown significantly inhibits differentiation of C2C12 myoblasts. These include known regulators of myogenesis (Myod1, Myog and Myf5), as well as 26 regulators not previously associated with the process. Of the TRs differentially expressed within the first 24 hours, two-thirds inhibited differentiation when knocked down. Surprisingly, a similar proportion (67%) of shRNAs targeting TRs whose expression did not change during differentiation also inhibited myogenesis, suggesting that both stably and differentially expressed TRs are essential for this complex differentiation program. This implies that microarray-based approaches that concentrate functional validation studies on differentially-expressed genes will fail to identify many genes that are critically implicated in complex biological processes. C2C12 myoblasts were differentiated into myotubes and sampled at various time points for gene expression measurement on MOE-430v2 chips. Cells grown in separate plates were harvested at 14 different time points: t_-24h, t_0h, t_0.5h, t_1h, t_1.5h, t_2h, t_3h, t_6h, t_9h, t_12h, t_24h, t_48h, t_96h, t_144h. Cells were also pre-treated with 50uM cycloheximide 1 hour prior to inducing differentiation and harvested at two time points: t_chx_1h, t_chx_3h. All harvests were performed in triplicate using growths from successive passages.
2012-03-21 | E-GEOD-16992 | biostudies-arrayexpress
Project description:We identified a novel muscle-specific lncRNA, lncFAM71E1-2:2 (lncFAM), which increased robustly during early human myogenesis. Overexpression of lncFAM promoted differentiation of human myoblasts into myotubes, while silencing lncFAM suppressed this process. A nucleus-resident lncRNA, lncFAM was studied using chromatin isolation by RNA purification followed by mass spectrometry (ChIRP-ms) analysis to identify the molecular mechanisms whereby it might promote myogenesis. Analysis of lncFAM-interacting proteins revealed that lncFAM recruited the RNA-binding protein HNRNPL to the promoter of MYPBPC2, in turn increasing MYBPC2 mRNA transcription and enhancing production of the myogenic protein MYPBPC2. These results highlight a mechanism whereby a novel ribonucleoprotein complex, lncFAM-HNRNPL promotes MYBPC2 expression transcriptionally to increase myogenesis.
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