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Transcriptional profiling of PRDM2 Knock down vs.controlGFPsh Quiescent C2C12 Myoblasts (G0 enriched)

ABSTRACT: Knockdown of PRDM2 led to precocious differentiation. To understand the molecular basis for this phenotype, we performed microaary analysis of quiescent myoblasts. Genes differentially regulated by PRDM2 knock down were reveraled by microarray analysis using affymetrix mouse chips.

ORGANISM(S): Mus musculus

PROVIDER: GSE58674 | GEO | 2015/06/30

SECONDARY ACCESSION(S): PRJNA253139

REPOSITORIES: GEO

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Transcriptional profiling of PRDM2 Knock down vs.controlGFPsh Quiescent C2C12 Myoblasts (G0 enriched)

Project description:Knockdown of PRDM2 led to precocious differentiation. To understand the molecular basis for this phenotype, we performed microaary analysis of quiescent myoblasts. Genes differentially regulated by PRDM2 knock down were reveraled by microarray analysis using affymetrix mouse chips. Control and knock down cells were synchronized at G0 by suspension culture and total RNA was used to perform microarray analysis

2015-06-30 | E-GEOD-58674 | biostudies-arrayexpress

Transcriptional profiling of PRDM2 Knock down vs.controlGFPsh proliferating C2C12 Myoblasts

Project description:Knockdown of PRDM2 led to precocious differentiation. To understand the molecular basis for this phenotype, we performed microaary analysis of growing myoblasts. Genes differentially regulated by PRDM2 knock down were reveraled by microarray analysis using NIA15K mouse chips.

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Transcriptional profiling of PRDM2 Knock down vs.controlGFPsh differentiated C2C12 Myoblasts (D28hrs)

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Project description:PRDM2 directly associates with the Myogenin promoter and repress its transcription. This led to the hypothesis that PRDM2 could potentially associate directly with other promoters and regulate their expression.To gain further insight into the pathways and genes controlled by PRDM2, ChIP-on-Chip analysis was performed using mouse 44K promoter array. Since PRDM2 represses transcription by H3K9 dimethylation, we were interested in determining which targets were occupied by PRDM2 as well as showed enrichment for H3K9me2. Hence ChIP-on-Chip analysis for H3K9me2 was performed to find the overlap between PRDM2 and H3K9me2 marked promoters.

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Project description:Quiescent stem cells contribute to tissue homeostasis and repair in adult mammals. We identified a tumor suppressor PRDM2, as an epigenetic regulator induced in quiescent muscle stem cells as well as in cultured quiescent myoblasts. To delineate the functions of PRDM2 in muscle cells, we compared the gene expression profiles of control and PRDM2 knockdown myoblasts in growing, differentiating and quiescent conditions (GEO accession number: GSE 58676). To identify the direct targets of PRDM2 and the promoters co-associated with H3K9me2 (mark catalyzed by PRDM2), ChIP-Chip analysis was performed (GSE58748). In this report we discuss in detail the methodology used to identify PRDM2 regulated genes and classify them into potential direct and indirect targets.

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Gene expression profiling of PRDM2 Knockdown in proliferating, quiescent and differentiating myoblasts

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Transcriptional profiling of MLL5 Knock down vs. control C2C12 myoblasts (S phase enriched)

Project description:Knockdown of MLL5 led to deregulation of S phase. To understand the molecular basis for this phenotype, we performed microarray analysis of S phase synchronized myoblasts. Genes differentially regulated by MLL5 knock down were revealed by microarray analysis using NIA15K mouse chips.

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