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Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional profiling by array of stable HeLa cell line with doxycycline-inducible transcription factor E2F7 transgene

ABSTRACT: stable dox-inducible HeLa lines expressing E2F7

ORGANISM(S): Homo sapiens

SUBMITTER: M Groot Koerkamp

PROVIDER: E-TABM-1212 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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E2F7 represses a network of oscillating cell cycle genes to control S-phase progression.

Westendorp Bart B Mokry Michal M Groot Koerkamp Marian J A MJ Holstege Frank C P FC Cuppen Edwin E de Bruin Alain A

Nucleic acids research 20111217 8

E2F transcription factors are known to be important for timely activation of G(1)/S and G(2)/M genes required for cell cycle progression, but transcriptional mechanisms for deactivation of cell cycle-regulated genes are unknown. Here, we show that E2F7 is highly expressed during mid to late S-phase, occupies promoters of G(1)/S-regulated genes and represses their transcription. ChIP-seq analysis revealed that E2F7 binds preferentially to genomic sites containing the TTCCCGCC motif, which closely ...[more]

PMID: 22180533

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RASSF1A promotes its tumor-suppressive function via YAP1 target genes

Project description:The aim of the study was to determine the effect of the tumour suppressor RASSF1A in a stably induced YAP system, as both are members of the growth regulatory HIPPO pathway. YAP1 expression was induced by Doxycycline in stably transfected HEK293 cells. In addition the cells were transfected with RASSF1A/GFP or GFP. Transfected cells were FACS-sorted by the GFP-signal and lysed for transcriptome analysis.

2017-05-15 | E-MTAB-4781 | biostudies-arrayexpress

Genome-wide analysis reveals NRP1 as a critical HIF1-E2F7 target gene in the regulation of motorneuron guidance in vivo

Project description:HIF1 is essential for regulation of the transcriptional response to hypoxia. Recently we showed that the transcriptional repressors E2F7 and E2F8 interact and transcriptionally cooperate with HIF1. Here we further explored this cooperation by performing genome-wide analysis, screening for novel HIF1-E2F7 targets. We show that specifically E2F7 is induced in hypoxia by HIF1. Furthermore, chip-sequencing for E2F7 and HIF1 revealed a large number of common targets of which a subset was also regulated by the complex as examined by microarray analysis. Our data show that the HIF1-E2F7 complex can function both as a repressor or activator. Notably, we identify neuropilin 1 (NRP1) as a novel HIF1-E2F7 target, which is repressed by HIF1-E2F7 in vitro and during zebrafish development, depending on E2F-binding sites present in the NRP1 promoter. In addition we show that regulation of NRP1 by the HIF1-E2F7 complex is required for normal axon guidance of spinal motorneurons in vivo. ChIP-seq analysis of HIF1a and E2F7 binding

2015-12-11 | E-GEOD-66956 | biostudies-arrayexpress

WB001A: Genome-wide analysis reveals NRP1 as a critical HIF1-E2F7 target gene in the regulation of motor neuron guidance in vivo

Project description:In this study, we explored the existence of a transcriptional network co-regulated by E2F7 and HIF1Î±, as we show that expression of E2F7, like HIF1Î±, is induced in hypoxia, and because of the previously reported ability of E2F7 to interact with HIF1Î±. Our genome-wide analysis uncovers a transcriptional network that is directly controlled by HIF1Î± and E2F7, and demonstrates both stimulatory and repressive functions of the HIF1Î± -E2F7 complex. Among this network we reveal Neuropilin 1 (NRP1) as a HIF1Î±-E2F7 repressed gene. By performing in vitro and in vivo reporter assays we demonstrate that the HIF1Î±-E2F7 mediated NRP1 repression depends on a 41 base pairs 'E2F-binding site hub', providing a molecular mechanism for a previously unanticipated role for HIF1Î± in transcriptional repression. To explore the biological significance of this regulation we performed in situ hybridizations and observed enhanced nrp1a expression in spinal motorneurons (MN) of zebrafish embryos, upon morpholino-inhibition of e2f7/8 or hif1Î±. Consistent with the chemo-repellent role of nrp1a, morpholino-inhibition of e2f7/8 or hif1Î± caused MN truncations, which was rescued in TALEN-induced nrp1a(hu10012) mutants, and phenocopied in e2f7/8 mutant zebrafish. Therefore, we conclude that repression of NRP1 by the HIF1Î±-E2F7 complex regulates MN axon guidance in vivo. The following samples were analyzed by microarrays: RNA isolated from HeLa cells transfected with either control (scr), E2F7, HIF1a, E2F7 and E2F8, or E2F7 and HIF1a siRNAs. Cells were harvested 48h after transfection, and were grown the last 16h in hypoxia. RNA isolated from scr-transfected, normoxic HeLa cells was used as common reference RNA. Within each group of two biological replicates, sample versus common reference hybridisations were performed in balanced dye-swap. Microarrays used were human whole genome gene expression microarrays V1 (Agilent, Belgium).

2016-01-04 | E-GEOD-66750 | biostudies-arrayexpress

E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells

Project description:This SuperSeries is composed of the following subset Series: GSE32353: Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells (nCounter) GSE32354: Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null liver (Affymetrix) Refer to individual Series

2012-08-31 | E-GEOD-32355 | biostudies-arrayexpress

Genome wide maps of E2F7 binding in IMR90 cells

Project description:Oncogene-induced senescence is an anti-proliferative stress response program that acts as a fail-safe mechanism to limit oncogenic transformation and is regulated by the retinoblastoma protein (RB) and p53 tumor suppressor pathways. We identify the atypical E2F family member E2F7 as the only E2F transcription factor potently upregulated during oncogene-induced senescence, a setting where it acts in response to p53 as a direct transcriptional target. Once induced, E2F7 binds and represses a series of E2F target genes and cooperates with RB to efficiently promote cell cycle arrest and limit oncogenic transformation. Disruption of RB triggers a further increase in E2F7, which induces a second cell cycle checkpoint that prevents unconstrained cell division despite aberrant DNA replication. Mechanistically, E2F7 compensates for the loss of RB in repressing mitotic E2F target genes.

2012-08-25 | GSE40343 | GEO

Genome wide maps of E2F7 binding in IMR90 cells

2012-08-25 | E-GEOD-40343 | biostudies-arrayexpress

BW001: E2F7 represses a network of oscillating cell cycle genes to control S-phase progression

Project description:E2F transcription factors are known to be important for timely activation of G1/S and G2/M genes required for cell cycle progression, but transcriptional mechanisms for deactivation of cell cycle-regulated genes are unknown. Here, we show that E2F7 is highly expressed during mid to late S-phase, occupies promoters of G1/S-regulated genes and represses their transcription. ChIP-seq analysis revealed that E2F7 binds preferentially to genomic sites containing the TTCCCGCC motif, which closely resemble the E2F consensus site. We identified 89 target genes that carry E2F7 binding sites close to the transcriptional start site and that are directly repressed by short term induction of E2F7. Most of these target genes are known to be activated by E2Fs and are involved in DNA replication, metabolism and DNA repair. Importantly, induction of E2F7 during G0-G1/S resulted in S-phase arrest and DNA damage, whereas expression of E2F7 during G2/M failed to disturb cell cycle progression. These findings provide strong evidence that E2F7 directly controls the downswing of oscillating G1/S genes during S-phase progression.

2012-05-01 | GSE33448 | GEO

E2F7 represses a transcriptional network of oscillating cell cycle genes to control S-phase progression.

Project description:E2F transcription factors are known to be important for timely activation of G1/S and G2/M genes required for cell cycle progression, but transcriptional mechanisms for deactivation of cell cycle regulated genes are unknown. Here, we show that E2F7 is highly expressed during mid to late S-phase, occupies promoters of G1/S regulated genes and represses its transcription. ChIP-seq analysis revealed that E2F7 binds preferentially to genomic sites containing the TTCCCGCC motif, which closely resemble the E2F consensus site. We identified 89 target genes that carry E2F7 binding sites close to the transcriptional start site and that are directly repressed by short term induction of E2F7. Most of these target genes are known to be activated by E2Fs and are involved in DNA replication, metabolism and DNA repair. Importantly, induction of E2F7 during G0-G1/S resulted in S-phase arrest and DNA damage, whereas expression of E2F7 during G2/M failed to disturb cell cycle progression. These findings provide strong evidence that E2F7 controls directly the downswing of oscillating G1/S genes during S-phase progression.

2012-01-04 | GSE32673 | GEO

Expression data from Î²-globin let7 HeLa tet off cells treated with doxycycline

Project description:We used microarray to determine the genes whose expression was changed at six hours after doxycycline treatment Cells were transfected with Î²-globin let7 wt constructs. Two-condition experiment; HeLa tet off cells overexpressed control vs HeLa tet off cells treated with doxycycline for six hours

2016-03-15 | E-GEOD-66541 | biostudies-arrayexpress

SAPCD2 promotes neuroblastoma progression by altering the subcellular distribution of E2F7

Project description:We report a previously unrecognized role of SAPCD2 in E2F signaling pathway in neuroblastoma. To explore SAPCD2-dependent gene regulation, RNA-seq analysis was conducted and the differently expressed genes were revealed in the SAPCD2-knockdown SK-N-BE(2) cells in comparison to control group. We find that SAPCD2 contributes to E2F7 mislocalization and decreases the level of nuclear E2F7 in NB cells, thus restraining the inhibitory effect of nuclear E2F7 on E2F signaling pathway. SAPCD2 knockdown limits the overactivation of E2F signaling in NB cells, affects the expression of genes involved in cell cycle and chromosome stability, and thereby blocking tumor progression.

2022-01-23 | GSE186245 | GEO

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