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ChIP-chip from pregnant female mouse pituitary with POU1F1 (PIT-1)

ABSTRACT: POU1F1 regulates, in the pituitary, the development of the prolactin-, growth hormone- and thyrotropin ß-expressing lineages and the expression of these hormone in the mature pituitary through the direct regulation of their promoters. Besides these functions, POU1F1 is also involved in other cellular processes in the pituitary, such as cell division and survival, but the genomic targets involved in these actions are not known. The present ChIP-chip study identified a large number of hitherto unknown potential direct targets that might be involved in these actions, such as Tcf4, Lmo4, Pax6, Trp53 etc. ChIP-chip was done from pregnant female mouse (C57Bl/6J) pituitary (3 pools of 12 pituitary anterior lobes, corresponding to three biological replicates) with POU1F1 (PIT-1)

ORGANISM(S): Mus musculus

SUBMITTER: Jean-Paul Herman

PROVIDER: E-GEOD-33318 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ChIP-chip from pregnant female mouse pituitary with POU1F1 (PIT-1)

Project description:POU1F1 regulates, in the pituitary, the development of the prolactin-, growth hormone- and thyrotropin ß-expressing lineages and the expression of these hormone in the mature pituitary through the direct regulation of their promoters. Besides these functions, POU1F1 is also involved in other cellular processes in the pituitary, such as cell division and survival, but the genomic targets involved in these actions are not known. The present ChIP-chip study identified a large number of hitherto unknown potential direct targets that might be involved in these actions, such as Tcf4, Lmo4, Pax6, Trp53 etc.

2011-10-29 | GSE33318 | GEO

ChIP-chip from mouse male and female adult livers and P12.5 embryos with H3K27me3

Project description:The H3K27me3 is a repressive histone mark associated with repressive chromatin and is important for X chromosome inactivation. ChIP-chip of H3K27me3 along the mouse X chromosome in male and female livers and p12.5 embryos demonstrated that H3K27me3 is absent at the genes that escape X inactivation. Comparison of H3K27me3 enrichment along the X chromosome in male and female adult livers and P12.5 embryos

2010-03-04 | E-GEOD-20617 | biostudies-arrayexpress

G9a selectively represses a class of late-replicating genes at the nuclear periphery (Expression)

Project description:We have investigated the role of the histone methyltransferase G9a in the establishment of silent nuclear compartments. Following conditional knockout of the G9a methyltransferase in mouse ESCs, 167 genes were significantly up-regulated, and no genes were strongly down-regulated. A partially overlapping set of 119 genes were up-regulated after differentiation of G9a-depleted cells to neural precursors. Promoters of these G9a-repressed genes were AT rich and H3K9me2 enriched but H3K4me3 depleted and were not highly DNA methylated. Representative genes were found to be close to the nuclear periphery, which was significantly enriched for G9a-dependent H3K9me2. Strikingly, although 73% of total genes were early replicating, more than 71% of G9a-repressed genes were late replicating, and a strong correlation was found between H3K9me2 and late replication. However, G9a loss did not significantly affect subnuclear position or replication timing of any non-pericentric regions of the genome, nor did it affect programmed changes in replication timing that accompany differentiation. We conclude that G9a is a gatekeeper for a specific set of genes localized within the late replicating nuclear periphery. 4 cell states each in duplicate (i.e. a total of 8 individual replicates)

2010-06-20 | E-GEOD-18076 | biostudies-arrayexpress

Replication-Timing Boundaries Facilitate Cell-type and Species-specific Regulation of a Rearranged Human Chromosome in Mouse

Project description:In multicellular organisms, developmental changes to replication timing occur in 400- 800 kb domains across half the genome. While clear examples of epigenetic control of replication timing have been described, a role for DNA sequence in mammalian replication timing has not been substantiated. To assess the role of DNA sequences in directing these changes, we profiled replication timing in mice carrying a genetically rearranged Human Chromosome 21 [Hsa21]. In two distinct mouse cell types, Hsa21 sequences maintained human-specific replication timing, except at points of Hsa21 rearrangement. Changes in replication timing at rearrangements extended up to 900 kb and consistently reconciled with the wild-type replication pattern at developmental boundaries of replication-timing domains. Our results demonstrate DNA sequencedriven regulation of Hsa21 replication timing during development and provide evidence that mammalian chromosomes consist of multiple independent units of replication timing regulation. Profile comparison of fibroblast and T-cell cultures from trans-chromosomic mice and human and mouse controls.

2012-06-04 | E-GEOD-38472 | biostudies-arrayexpress

G9a selectively represses a class of late-replicating genes at the nuclear periphery

Project description:This SuperSeries is composed of the following subset Series: GSE18076: G9a selectively represses a class of late-replicating genes at the nuclear periphery (Expression) GSE18079: G9a selectively represses a class of late-replicating genes at the nuclear periphery (WG_CGH) Refer to individual Series

2009-11-02 | E-GEOD-18082 | biostudies-arrayexpress

Mutant p53 cooperates with ETS2 to promote etoposide resistance [ChIP-chip]

Project description:Mutant p53 (mtp53) promotes chemotherapy resistance through multiple mechanisms including disabling pro-apoptotic proteins and by regulating gene expression. Analysis of promoter regions identified through CHIP-on-CHIP and CHIP-SEQ platforms reveal that the ETS motif (EBS) is prevalent within predicted mtp53 binding sites. We demonstrate that mtp53 regulates gene expression through EBS in promoters, and that ETS2 mediates the interaction with this motif. Importantly, we identified TDP2, a 5’-tyrosyl DNA phosphodiesterase involved in the repair of DNA damage caused by etoposide, as a transcriptional target of mtp53. We demonstrate that suppression of TDP2 sensitizes mtp53 expressing cells to etoposide, and that mtp53 and TDP2 are frequently overexpressed in human lung cancer; thus, our analysis identifies a potentially “druggable” component of mtp53’s gain-of-function activity. Comparison of two different transcriptional binding analysis (ChIP-on-ChIP and ChIP-Seq) for the identification of novel mutant p53 (R248W) binding.

2012-05-02 | E-GEOD-36751 | biostudies-arrayexpress

Genome-Wide Dynamics of Replication Timing Revealed by In Vitro Models of Mouse Embryogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE17980: Genome-Wide Dynamics of Replication Timing Revealed by In Vitro Models of Mouse Embryogenesis (Expression) GSE17983: Genome-Wide Dynamics of Replication Timing Revealed by In Vitro Models of Mouse Embryogenesis (WG_CGH; Replication Timing) GSE17980 (Expression): 8 cell lines, with a total of 14 individual replicates (i.e. 6 in duplicates, 2 in single replicates) GSE17983 (WG_CGH; Replication Timing): 22 cell lines, with a total of 36 individual replicates (i.e. 14 in duplicates, 8 in single replicates)

2010-05-19 | E-GEOD-18019 | biostudies-arrayexpress

Replication timing profiling by Repli-chip in Mus musculus

Project description:The replication timing program, or the order in which DNA is duplicated during S-phase, is associated with various features of chromosome structure and function, including gene expression, histone modifications, and 3-D compartmentalization of chromatin. 3 cell types, with a total of 6 individual replicates

2013-04-16 | E-GEOD-45716 | biostudies-arrayexpress

The distribution of genomic variations in human iPSCs is related to replication timing reorganization during reprogramming [NimbleGen]

Project description:Cell fate change involves significant genome reorganization, including change in replication timing, but how these changes are related to genetic variation has not been examined. To study how change in replication timing that occurs during reprogramming impacts the copy number variation (CNV) landscape, we generated genome-wide replication timing profiles of induced pluripotent stem cells (iPSCs) and their parental fibroblasts. A significant portion of the genome changes replication timing as a result of reprogramming, indicative of overall genome reorganization. We found that early and late replicating domains in iPSCs are differentially affected by copy number gains and losses, and that in particular CNV gains accumulate in regions of the genome that change to earlier replication during the reprogramming process. This differential relationship was present irrespective of reprogramming method. Overall, our findings reveal a functional association between reorganization of replication timing and the CNV landscape that emerges during reprogramming. 3 cell lines, all in duplicates

2014-03-28 | E-GEOD-55397 | biostudies-arrayexpress

Influence of ATM-mediated DNA damage response on genomic variation in human induced pluripotent stem cells (NimbleGen CNV)

Project description:Genome instability is a potential limitation to the research and therapeutic application of induced pluripotent stem cells (iPSCs). Observed genomic variations reflect the combined activities of DNA damage, cellular DNA damage response (DDR), and selection pressure in culture. To understand the contribution of DDR on the distribution of copy number variations (CNVs) in iPSCs, we mapped CNVs of iPSCs with mutations in the central DDR gene ATM onto genome organization landscapes defined by genome-wide replication timing profiles. We show that following reprogramming the early and late replicating genome is differentially affected by CNVs in ATM deficient iPSCs relative to wild type iPSCs. Specifically, the early replicating regions had increased CNV losses during retroviral reprogramming. This differential CNV distribution was not present after later passage or after episomal reprogramming. Comparison of different reprogramming methods in the setting of defective DNA damage response reveals unique vulnerability of early replicating open chromatin to retroviral vectors. 4 cell lines, all in duplicates

2016-03-29 | E-GEOD-78717 | biostudies-arrayexpress

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