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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Sirisha Cheedipudi

PROVIDER: E-GEOD-58676 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

A fine balance: epigenetic control of cellular quiescence by the tumor suppressor PRDM2/RIZ at a bivalent domain in the cyclin a gene.

Cheedipudi Sirisha S Puri Deepika D Saleh Amena A Gala Hardik P HP Rumman Mohammed M Pillai Malini S MS Sreenivas Prethish P Arora Reety R Sellathurai Jeeva J Schrøder Henrik Daa HD Mishra Rakesh K RK Dhawan Jyotsna J

Nucleic acids research 20150603 13

Adult stem cell quiescence is critical to ensure regeneration while minimizing tumorigenesis. Epigenetic regulation contributes to cell cycle control and differentiation, but few regulators of the chromatin state in quiescent cells are known. Here we report that the tumor suppressor PRDM2/RIZ, an H3K9 methyltransferase, is enriched in quiescent muscle stem cells in vivo and controls reversible quiescence in cultured myoblasts. We find that PRDM2 associates with >4400 promoters in G0 myoblasts, 5 ...[more]

PMID: 26040698

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

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2015-06-30 | E-GEOD-58675 | biostudies-arrayexpress

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

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2013-04-01 | E-GEOD-44119 | biostudies-arrayexpress

eRNAs Promote Transcription by Establishing Chromatin Accessibility at Defined Genomic Loci

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2011-11-23 | E-GEOD-25549 | biostudies-arrayexpress

A KAP1 phosphorylation switch controls MyoD function during skeletal muscle differentiation (ChIP-seq)

Project description:The transcriptional activator MyoD serves as a master controller of myogenesis. Often in partnership with Mef2, MyoD binds to the promoters of hundreds of muscle genes in proliferating myoblasts, yet activates these targets only upon receiving cues that launch differentiation. What regulates this off/on switch of MyoD function has been incompletely understood, although known to reflect the action of chromatin modifiers. Here, we identify KAP1/TRIM28 as a key regulator of MyoD function. In myoblasts, KAP1 is present with MyoD and Mef2 at many muscle genes, where it acts as a scaffold to recruit not only co-activators such as p300 and LSD1, but also co-repressors such as G9a and HDAC1, with promoter silencing as net outcome. Upon differentiation, MSK1-mediated phosphorylation of KAP1 releases the co-repressors from the scaffold, unleashing transcriptional activation by MyoD/Mef2 and their positive cofactors. Thus, our results reveal KAP1 as a previously unappreciated interpreter of cell signaling, which modulates the ability of MyoD to drive myogenesis. Kap1 and H3K9me3 ChIPseq in proliferating C2C12 cells

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