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Genome-wide maps of chromatin state in mouse erythroid cells.

ABSTRACT: We generated genome-wide chromatin state and RNA Polymerase II binding maps in mouse erythroid cells by ChIP-Seq. Examination of 4 different histone modifications (H3K4me3, H3K4me1, H3K27me3, H3K27ac) and RNA Polymerase II (RNAP2) binding in mouse erythroid cells (Ter119+).

ORGANISM(S): Mus musculus

SUBMITTER: Monika Kowalczyk

PROVIDER: E-GEOD-27918 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Intragenic enhancers act as alternative promoters.

Kowalczyk Monika S MS Hughes Jim R JR Garrick David D Lynch Magnus D MD Sharpe Jacqueline A JA Sloane-Stanley Jacqueline A JA McGowan Simon J SJ De Gobbi Marco M Hosseini Mona M Vernimmen Douglas D Brown Jill M JM Gray Nicola E NE Collavin Licio L Gibbons Richard J RJ Flint Jonathan J Taylor Stephen S Buckle Veronica J VJ Milne Thomas A TA Wood William G WG Higgs Douglas R DR

Molecular cell 20120119 4

A substantial amount of organismal complexity is thought to be encoded by enhancers which specify the location, timing, and levels of gene expression. In mammals there are more enhancers than promoters which are distributed both between and within genes. Here we show that activated, intragenic enhancers frequently act as alternative tissue-specific promoters producing a class of abundant, spliced, multiexonic poly(A)(+) RNAs (meRNAs) which reflect the host gene's structure. meRNAs make a substan ...[more]

PMID: 22264824

Similar Datasets

Intragenic enhancers act as alternative promoters

Project description:This SuperSeries is composed of the following subset Series: GSE26877: Nprl3 is Required for Normal Development of the Cardiovascular System GSE27918: Genome-wide maps of chromatin state in mouse erythroid cells. GSE27919: Genome-wide map of DNaseI hypersensitivity in mouse erythroid cells. GSE27920: Transcriptiome of mouse erythroid cells (part2) Refer to individual Series

2012-01-30 | E-GEOD-27921 | biostudies-arrayexpress

Genome-wide maps of chromatin modifications in C57bl\6 mouse erythroid cells.

Project description:Regions of chromatin modified by H3K4me1 and H3K4me3 were identified in mouse erythroid cells using ChIP-seq. Chip-seq experiements were performed in C57bl\6 mouse erythroid Ter119+ cells.

2013-11-11 | E-GEOD-49455 | biostudies-arrayexpress

Genome-wide maps of transcriptional factor binding in mouse erythroid cells.

Project description:Regions bound by the erythroid transcription factors GATA1 and NFE2 and the general factor CTCF were identified in mouse erythroid cells using ChIP-seq. Chip-seq experiements were performed in mouse erythroid Ter119+ cells.

2013-12-21 | E-GEOD-47492 | biostudies-arrayexpress

Genome-wide ChIP seq of H3.3 in WT and ATRX KO mouse ES cells

Project description:Regions of H3.3 binding in WT and ATRX KO mouse ES cells were identified by ChIP seq Chip-seq experiements were performed in WT and ATRX KO E14 mouse ES cells

2015-04-16 | E-GEOD-59270 | biostudies-arrayexpress

Chromatin signatures at transcriptional start sites separate two equally populated yet distinct classes of intergenic long noncoding RNAs

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

2013-11-11 | E-GEOD-49460 | biostudies-arrayexpress

WT and ATRX KO

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

2015-04-16 | E-GEOD-59271 | biostudies-arrayexpress

A comparison of control samples for ChIP-seq of histone modifications

Project description:The advent of high-throughput sequencing has allowed genome wide profiling of histone modifications by Chromatin ImmunoPrecipitation (ChIP) followed by sequencing (ChIP-seq). In this assay the histone mark of interest is enriched through a chromatin pull-down assay using an antibody for the mark. Due to imperfect antibodies and other factors, many of the sequenced fragments do not originate from the histone mark of interest, and are referred to as background reads. Background reads are not uniformly distributed and therefore control samples are usually used to estimate the background distribution at any given genomic position. The Encyclopedia of DNA Elements (ENCODE) Consortium guidelines suggest sequencing a whole cell extract (WCE, or “input”) sample, or a mock ChIP reaction such as an IgG control, as a background sample. However, for a histone modification ChIP-seq investigation it is also possible to use a Histone H3 (H3) pull-down to map the underlying distribution of histones. In this paper we generated data from a hematopoietic stem and progenitor cell population isolated from mouse foetal liver to compare WCE and H3 ChIP-seq as control samples. The quality of the control samples is estimated by a comparison to pull-downs of histone modifications and to expression data. We find minor differences between WCE and H3 ChIP-seq, such as coverage in mitochondria and behaviour close to transcription start sites. Where the two controls differ, the H3 pull-down is generally more similar to the ChIP-seq of histone modifications. However, the differences between H3 and WCE have a negligible impact on the quality of a standard analysis. WCE and histone H3 ChIP-seq samples are compared to H3K27me3 ChIP-seq and RNA-seq.

2015-01-01 | E-GEOD-59419 | biostudies-arrayexpress

ChIP-chip by array of human B-acute lymphoblastic leukaemia cells using AcH3, H3K4M3 and H3K27M3 antibodies

Project description:B-ALL Xenograft Histone Modification at BIM locus<br>The cells used are human B- acute lymphoblastic leukaemia cells that have been propagated in<br>NOD/SCID mice. B-ALL2 and B-ALL3 are cells from two different patients.<br><br>Normalized data files containing chromosome 2 data are available on the FTP site for this experiment in the E-MEXP-2814.additional.zip archive.

2011-06-14 | E-MEXP-2814 | biostudies-arrayexpress

ChIP-chip by array of human T-acute lymphoblastic leukaemia cells using AcH3 antibodies

Project description:T-ALL Xenograft Histone Modification at ERG locus: The cells used are human T-acute lymphoblastic leukaemia cells that have been propagated in NOD/SCID mice. T-ALL8,T-ALL16, T-ALL27, T-ALL29, T-ALL30 and T-ALL31 are cells from six different patients. Normalized data files containing chromosome 21 data are available on the FTP site for this experiment in the E-MTAB-431.additional.zip archive.

2012-01-01 | E-MTAB-431 | biostudies-arrayexpress

Cpeb4-mediated Translational Regulatory Circuitry Controls Terminal Erythroid Differentiation

Project description:Erythropoiesis is essential to mammals and is regulated at multiple steps by both extracellular and intracellular factors. Many transcriptional regulatory networks in erythroid differentiation have been well characterized. However, our understanding of post-transcriptional regulatory circuitries in this developmental process is still limited. Using genomic approaches, we identified a sequence-specific RNA-binding protein, Cpeb4, which is dramatically induced in terminal erythroid differentiation (TED) by two erythroid important transcription factors, Gata1/Tal1. Cpeb4 belongs to the cytoplasmic polyadenylation element binding (CPEB) protein family that regulates translation of target mRNAs in early embryonic development, neuronal synapse, and cancer. Using primary mouse fetal liver erythroblasts, we found that Cpeb4 is required for terminal erythropoiesis by repressing the translation of a set of mRNAs highly expressed in progenitor cells. This translational repression occurs by the interaction with a general translational initiation factor, eIF3. Interestingly, Cpeb4 also binds its own mRNA and represses its translation, thus forming a negative regulatory circuitry to limit Cpeb4 protein level. This mechanism ensures that the translation repressor, Cpeb4, does not interfere with the translation of other mRNAs in differentiating erythroblasts. Our study characterized a translational regulatorycircuitry that controls TED and revealed that Cpeb4 is required for somatic cell differentiation. We used microarray to identify mRNAs associated with Cpeb4 in mouse fetal liver erythroblasts. Cpeb4 associated mRNAs were isolated from mouse fetal liver erythroblasts using anti-Cpeb4 antibody for immunoprecipitation followed by RNA extraction. Then Affymetrix microarrays were used to identify and quantify the mRNAs associated with Cpeb4.

2015-12-09 | E-GEOD-57004 | biostudies-arrayexpress

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