H3K27me3 profiles along the length of the X chromosome in trophoblast stem (TS) cells showing inverted X-inactivation profiles, ChIP-chip
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Celine Morey
PROVIDER: E-GEOD-68536 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:This analysis includes H3K27me3 and H3K4me2 profiles along the length of the X-chromosome in male (F2) and female (F3) TS cells and in male (GHP7/7) and female (GHP7/9) XEN cells. Analysis of H3K27me3 and H3K4me2 profiles in four different cell populations. Two independent biological replicates for each cell population are provided. The array includes approx. 162,5 Mb of the X chromosome and approx. 14,6 Mb of chromosome 17 as a control.
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Project description:This analysis includes H3K27me3 profiles along the length of the X-chromosome in male (F2) and female (K4) TS cells and in female TS cells showing local reversals of imprinted X-chromosome inactivation (K4GFP). Data also includes H3K27me3 ChIP-chip profiles in Eed-/- mutant male and female TS cells obtained from Magnuson laboratory (Kalantry S. et al., Nat Cell Biol, 2006). Analysis of H3K27me3 profiles in five different cell populations. Three independent biological replicates for each wild-type female cell population and two independent biological replicates for the wild-type male cell population are provided. The ChIP-chip analysis was also carried out in Eed-/- male and female TS cells lacking H3K27me3 for comparison (one replicate). The array includes approx. 162,5 Mb of the X chromosome and approx. 14,6 Mb of chromosome 17 as a control.
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Project description:In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics, C. elegans ChIP-chip with DPY-27
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2014-02-26 | E-MTAB-2343 | biostudies-arrayexpress
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
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Project description:Two chromosome-targeting and gene regulatory systems are present in Drosophila melanogaster. The male X-chromosome is targeted by the male-specific lethal complex believed to mediate the two-fold up-regulation of the X-linked genes. The highly heterochromatic 4th chromosome is specifically targeted by the Painting of Fourth (POF) protein which together with heterochromatin protein 1 (HP1) modulate the expression level of genes on the 4th chromosome. Here we report high-resolution mapping of POF and HP1 on the 4th chromosome using chromatin immunoprecipitation followed by tiling microarrays (ChIP-chip) in S2 cells and salivary glands. The enrichments are compared to transcript profiles of the two cell types used. POF specifically binds to genes with a strong preference for exons. The POF binding profile correlates to the binding profile of HP1 which in addition displays a typical M-bM-^@M-^\peakM-bM-^@M-^] in the promoter regions of bound genes. POF and HP1 binds to active genes and the binding correlates with levels of transcription and changes in binding levels are paralleled by a comparable change in transcription. Our results provide a high resolution description of the chromosome 4 specific gene regulatory system provided by the combinatorial effects of POF and HP1. Keywords: Transcript profiling Transcript profiling in S2 cells and salivary glands. Two biological replicates, one replicate per array.
2007-10-02 | E-GEOD-8297 | biostudies-arrayexpress
Project description:This analysis includes H3K27me3 and H3K4me2 profiles along the length of the X-chromosome in male (F2) and female (F3) TS cells and in male (GHP7/7) and female (GHP7/9) XEN cells.
2014-06-01 | GSE50587 | GEO
Project description:In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics, C. elegans ChIP-chip experiments included: biological duplicates of SDC-3 and MIX-1 IPs, a single DPY-27 IP, and 3 mock IPs.
2010-05-22 | E-GEOD-14650 | biostudies-arrayexpress
Project description:In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics, C. elegans ChIP-chip experiments included: biological duplicates of SDC-3, a single DPY-27 IP, and a mock IP.
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