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ChIP-chip analysis of human DREAM complex subunits in G0-arrested and S-phase synchronized cells

ABSTRACT: This experiment is a part of global location analysis of the human DREAM complex including subunits: E2F4, RBL2/p130, LIN9 and LIN54. Specifically, the regions in Human Promoter Array 1.0R (GPL5082) bound by: E2F4 in G0-arrested T98G cells E2F4 in S-phase synchronized T98G cells LIN54 in G0-arrested T98G cells LIN54 in S-phase synchronized T98G cells LIN9 in G0-arrested T98G cells LIN9 in S-phase synchronized T98G cells p130 in G0-arrested T98G cells p130 in S-phase synchronized T98G cells were compared with input chromatin. MAT (Model-based Analysis for Tiling Arrays) .bar and .bed output files provided as supplementary files. Keywords: CHiP-chip genomic DNA

ORGANISM(S): Homo sapiens

PROVIDER: GSE7516 | GEO | 2007/04/17

SECONDARY ACCESSION(S): PRJNA99415

REPOSITORIES: GEO

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Transcription profiling of human T98G cells during cell cycle in T98G

Project description:The mammalian Retinoblastoma (RB) family including pRB, p107, and p130 represses E2F target genes through mechanisms that are not fully understood. In D. melanogaster, RB-dependent repression is mediated in part by the multisubunit protein complex Drosophila RBF, E2F, and Myb (dREAM) that contains homologs of the C. elegans synthetic multivulva class B (synMuvB) gene products. Using an integrated approach combining proteomics, genomics, and bioinformatic analyses, we identified a p130 complex termed DP, RB-like, E2F, and MuvB (DREAM) that contains mammalian homologs of synMuvB proteins LIN-9, LIN-37, LIN-52, LIN-54, and LIN-53/RBBP4. DREAM bound to more than 800 human promoters in G0 and was required for repression of E2F target genes. In S phase, MuvB proteins dissociated from p130 and formed a distinct submodule that bound MYB. This work reveals an evolutionarily conserved multisubunit protein complex that contains p130 and E2F4, but not pRB, and mediates the repression of cell cycle-dependent genes in quiescence. Experiment Overall Design: Gene expression during the cell cycle in T98G cells. Cells were serum starved for 72 hours to induce G0 and then restimuated to enter cell cycle by serum addition. BrdU and FACS was done simultaneously to confirm their cell cycle phase.

2008-06-16 | E-GEOD-8537 | biostudies-arrayexpress

Homo sapiens

Project description:ChIP-chip analysis of human DREAM complex subunits in G0-arrested and S-phase synchronized cells

| PRJNA99415 | ENA

Gene expression profilie during cell cycle in T98G cells

Project description:The mammalian Retinoblastoma (RB) family including pRB, p107, and p130 represses E2F target genes through mechanisms that are not fully understood. In D. melanogaster, RB-dependent repression is mediated in part by the multisubunit protein complex Drosophila RBF, E2F, and Myb (dREAM) that contains homologs of the C. elegans synthetic multivulva class B (synMuvB) gene products. Using an integrated approach combining proteomics, genomics, and bioinformatic analyses, we identified a p130 complex termed DP, RB-like, E2F, and MuvB (DREAM) that contains mammalian homologs of synMuvB proteins LIN-9, LIN-37, LIN-52, LIN-54, and LIN-53/RBBP4. DREAM bound to more than 800 human promoters in G0 and was required for repression of E2F target genes. In S phase, MuvB proteins dissociated from p130 and formed a distinct submodule that bound MYB. This work reveals an evolutionarily conserved multisubunit protein complex that contains p130 and E2F4, but not pRB, and mediates the repression of cell cycle-dependent genes in quiescence. Keywords: Gene expression analysis during cell cycle

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The E2F4/p130 repressor complex cooperates with oncogenic Np73 to promote cell survival

Project description:Tumor suppressor p53 and its related proteins, p63 and p73, can be synthesized as multiple isoforms lacking part of the N- or C-terminal regions. Specifically, high expression of the Np73 isoform is notoriously associated with poor prognosis in cancer. Here, we have performed proteomics analysis of Np73 using as a cellular model human papillomavirus type 38-transformed keratinocytes (38HK) that express high levels of this isoform. We find that Np73 associates with the E2F4/p130 repressor complex through a direct interaction with E2F4. Remarkably, this interaction is favored by the N-terminal truncation of p73 characteristic of Np73 isoforms and is independent of the C-terminal splicing status. We show that the Np73-E2F4/p130 complex is recruited to the promoters of specific genes, thereby enforcing inhibition of their expression both in 38HK and in cancer-derived cell lines. Consistently, silencing of E2F4 in 38HK and in cancer cells resulted in induction of senescence. In conclusion, we have identified and characterized a novel transcriptional regulatory complex that exerts pro-proliferative functions in transformed cells

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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. Control and knock down cells were synchronized at G0 by suspension culture and reactivated to enter S phase by replating for 24hrs in growth medium.

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