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Gene expression profiling on C3H/10T1/2 fibroblasts during their myogenic conversion in case of Six4 ablation

ABSTRACT: In this study, we used C3H/10T1/2 cells, a well known model of myogenic conversion, to study the effect of Six4 knockdown on the expression of genes during fibroblasts to myocytes conversion induced by ectopic expression of MyoD We established C3H/10T1/2 cell line with stable Six4 knockdown by short hairpin RNA (shSix4) vs a control cell line (shLuc) and converted these cells into myogenic lineage by retroviral transduction of plasmid encoding Flag-MyoD-myc (pBABE-MyoD) or empty plasmid (pBABE). Cells were then induced to differentiate for 24 hours before RNA extraction.

ORGANISM(S): Mus musculus

SUBMITTER: Alexandre Blais

PROVIDER: E-GEOD-66319 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profiling on C3H/10T1/2 fibroblasts during their myogenic conversion in case of Six4 ablation

Project description:In this study, we used C3H/10T1/2 cells, a well known model of myogenic conversion, to study the effect of Six4 knockdown on the expression of genes during fibroblasts to myocytes conversion induced by ectopic expression of MyoD

2015-12-31 | GSE66319 | GEO

Mus musculus

Project description:Gene expression profiling on C3H/10T1/2 fibroblasts during their myogenic conversion in case of Six4 ablation

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Genome-wide map of Six4 in C2C12 cells 24 hours post-differentiation

Project description:In this study, we used ChIP-seq to map Six4 binding profile in different C2C12 cell lines 24 hours after differentiation (T24). We performed ChIP-seq using two different antibodies: anti-Flag antibody in Flag-Six4 C2C12 cell line or in parental C2C12 cells; a custom-made anti-Six4 antibody in shNS C2C12 cell line (a control cell line) or shSix4 C2C12 (C2C12 with stable Six4 knockdown using short hairpin RNA). We also performed ChIP-seq in parental C2C12 cells using normal rabbit IgG. We were able to identify Six4-bound loci in C2C12 T24 that were recognized by two different antibodies and showed a decrease in peak intensity in shSix4 C2C12 compared to shNS C2C12 cells. We established a C2C12 cell line with stable Six4 knockdown by short hairpin RNA (shSix4) vs. a control cell line (shNS). We also established a C2C12 cell line with stable expression of Flag-Six4-myc by infection of retroviruses expressing pBABE-Flag-Six4-myc (Flag-Six4 C2C12) vs. parental C2C12. We differentiate these cells for 24 hours before using them for ChIP-seq.

2015-12-31 | E-GEOD-66901 | biostudies-arrayexpress

Gene Expression Profiling of siRNA Knock-Down of Six1, Six4 and Myogenin in C2C12

Project description:Six1, Six4 and Myogenin are transcription factors that are known to be required for skeletal myogenesis. Currently, very little is known about the genes targeted by Six1 and Six4. Gene expression profiling when one or both transcription factors were knock-down by siRNA was performed to identify genes affected by their absence. We also hypothesized that Six1 and Six4 can work in cooperation with the myogenic regulatory factor (MRFs) family of transcription factors, such as Myogenin. Therefore, we performed the same type of experiment where the myogenin was knocked-down by siRNA to identify genes that are possibly regulated by the Six1 or Six4 in conjunction with Myogenin. C2C12 Myoblasts were transfected with siRNA against Six1, Six4, Six1 with Six4, Myogenin, or control 24h before start of differentiation. The cells were allowed to differentiate in differentiation medium for 24h and were harvested for gene expression profiling. Four replicates per siRNA were performed.

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Transcriptome sequencing analysis of MyoD-induced transdifferentiation in 10T1/2 fibroblasts using RNA-seq

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Label-free quantification (LFQ) analysis on skeletal muscle stem cells and reprogrammed skeletal muscle stem and progenitor cells

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2022-05-19 | PXD029379 | Pride

Homo sapiens

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Remodeling of white fat during browning involves YBX1 to drive thermogenic commitment

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Project description:Ribosomes have been suggested to directly control gene regulation, however regulatory roles for ribosomal RNA (rRNA) remain largely unexplored. Expansion segments (ESs) consist of multitudes of tentacle-like rRNA structures extending from the core ribosome in eukaryotes. ESs are remarkably variable in sequence and size across eukaryotic evolution with a largely unknown function. In characterizing ribosome binding to a regulatory element within a Homeobox (Hox) 5’ UTR, we unexpectedly identify a modular stem-loop within this element that binds to a single ES, ES9S. Here, we described the raw data of the relative quantification proteomic analysis using tandem mass tag mass spectrometry of the ribonucleoprotein (RNP) complexes enriched from affinity pulldown of the 4xS1m-aptamer fusion constructs with the lysate components of C3H/10T1/2 cells and mouse embryo. 4xS1m pulldown is performed by combining mouse Hoxa9 mRNA elements (P3 and P4) with C3H/10T1/2 cell lysates, and by combining a9 IRES180 and an unrelated viral IRES with E11.5 FVB mouse embryo lysates. The aptamer alone served as a negative control. RNPs in the eluate were released by RNAse A treatment and were subjected to TMT 6plex labelling.

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SNAIL is a key regulator of rhabdomyosarcoma progression and myogenic differentiation

Project description:Rhabdomyosarcoma (RMS) is a frequent non-epithelial tumor of soft tissue that originates from a myogenic differentiation defect. Expression of SNAIL transcription factor is elevated in the alveolar subtype of RMS, characterized by a low myogenic differentiation status and high aggressiveness. SNAIL affects RMS metastasis by reorganization of actin cytoskeleton, regulation of ezrin expression and chemotaxis to HGF and SDF-1. The differentiation of human RMS diminishes SNAIL level. SNAIL silencing completely abolishes the growth of human RMS xenotransplants. SNAIL inhibits myogenic differentiation of RMS by binding to the MYF5 promoter, suppressing its expression, displacing MYOD from canonical to alternative E-box sequences and regulating myomiRs expression. SNAIL silencing allows the re-expression of MYF5 and canonical MYOD binding, promoting RMS cell myogenic differentiation. These novel results open potential avenues for the development of innovative therapeutic strategies based on SNAIL silencing.

2020-07-14 | PXD006711 | Pride

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