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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide map of H3K4me3 in 12 day post-partum mouse spermatocytes

ABSTRACT: Here we characterize the genome-wide chromatin modification by PRDM9, a histone H3 lysine 4 methyltransferase. In order to detect PRDM9 binding sites we created coisogenic strains of mice differing only in the zinc finger array of PRDM9. One strain is C57BL/6J, which carries the Prdm9Dom2 allele, the other strain was created using genomic replacement and named B6.PRDM9Cst (also called KI), and contains the Prdm9Cst allele originally found in CAST/EiJ mice. Many H3K4me3 positions are common between strains and represent other methyltransferase activity (such as promoters), sites that are unique to one mouse strain likely represent the binding position of that allele of PRDM9. Identify PRDM9-dependent H3K4me3 sites by comparing modified chromatin from mice coisogenic for Prdm9.

ORGANISM(S): Mus musculus

SUBMITTER: Kenneth Paigen

PROVIDER: E-GEOD-52628 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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PRDM9 binding organizes hotspot nucleosomes and limits Holliday junction migration.

Baker Christopher L CL Walker Michael M Kajita Shimpei S Petkov Petko M PM Paigen Kenneth K

Genome research 20140306 5

In mammals, genetic recombination during meiosis is limited to a set of 1- to 2-kb regions termed hotspots. Their locations are predominantly determined by the zinc finger protein PRDM9, which binds to DNA in hotspots and subsequently uses its SET domain to locally trimethylate histone H3 at lysine 4 (H3K4me3). This sets the stage for double-strand break (DSB) formation and reciprocal exchange of DNA between chromatids, forming Holliday junctions. Here we report genome-wide analyses of PRDM9-dep ...[more]

PMID: 24604780

Similar Datasets

Genome-wide map of H3K4me3 and PRDM9-binding in 12 day post-partum mouse spermatocytes

Project description:PRDM9, a histone methyltransferase, initiates meiotic recombination by binding DNA at recombination hotspots and directing the position of DNA double-strand breaks (DSB). The DSB repair mechanism suggests that hotspots should eventually self-destruct, yet genome-wide recombination levels remain constant, a conundrum known as the hotspot paradox. To test if PRDM9 drives this evolutionary erosion, we compared activity of the Prdm9Cst allele in two Mus musculus subspecies, M.m. castaneus, in which Prdm9Cst arose, and M.m. domesticus, into which Prdm9Cst was introduced. Comparing these two strains, we find that haplotype differences at hotspots leads to qualitative and quantitative changes in PRDM9 binding and activity. Most variants affecting PRDM9Cst binding arose and were fixed in M.m castaneus, suppressing hotspot activity. Furthermore, M.m castaneus x M.m domesticus F1 hybrids exhibit novel hotspots, representing sites of historic evolutionary erosion. Together these data support a model where haplotype-specific PRDM9 binding directs biased gene conversion at hotspots, ultimately leading to hotspot erosion. Identify position of meiotic H3K4me3 from various sub-species of mice and F1 hybrids from crosses between subspecies. In addition, perform ChIP-seq analysis on the meiosis-specific methyltransferase PRDM9.

2015-01-13 | E-GEOD-60906 | biostudies-arrayexpress

Genome-wide map of H3K4me3 in HEK293 cells after PRDM9 expression

Project description:PRDM9 is a histone methyltransferase expressed in meiotic germ cells that determines the location of genetic recombination hotspots through binding of its allele-specific DNA binding domain. Here we characterize the genome-wide chromatin modification for two human PRDM9 alleles (A and C) in human cell lines. HEK293 cells were transfected with both alleles and an empty vector control. Resulting chromatin was subjected to H3K4me3 ChIP followed by high-throughput sequencing. We find that different PRDM9 allele largely modified chromatin in entirely different genomic regions in somatic cells determined by the protein's zinc-finger DNA binding domains. Many of the allele-specific peaks overlap sites of meiotic double-strand breaks found in vivo in human germ cells suggesting that transient expression of PRDM9 in somatic cells can reflect binding in vivo. Identify PRDM9-dependent H3K4me3 sites by comparing modified chromatin after expression of different human PRDM9 alleles in HEK293 cells.

2015-09-21 | E-GEOD-67673 | biostudies-arrayexpress

ChIP-seq analyses of 10 quorum sensing regulators in Pseudomonas aeruginosa

Project description:The Pseudomonas aeruginosa quorum-sensing (QS) systems contribute to bacterial homeostasis and pathogenicity. Although many regulators have been characterized to control the production of virulence factors and QS signaling molecules, its detailed regulatory mechanisms still remain elusive. Here, we performed chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-seq) on 10 key QS regulators. The direct regulation of these genes by corresponding regulator has been confirmed by Electrophoretic mobility shift assays (EMSAs) and quantitative real-time polymerase chain reactions (qRT-PCR). Binding motifs are found by using MEME suite and verified by footprint assays in vitro. Collectively, this work provides new cues to better understand the detailed regulatory networks of QS systems. ChIP-seq of 10 QS regulators in Pseudomonas aeruginosa

2015-08-04 | E-GEOD-65356 | biostudies-arrayexpress

Supression of genetic recombination in the pseudoautosomal region and at subtelomeres in mice with a hypomorphic spo11 allele

Project description:Homologous recombination is the key process that generates genetic diversity and drives evolution. SPO11 protein triggers recombination by introducing DNA double stranded breaks at discreet areas of the genome called recombination hotspots. The hotspot locations are largely determined by the DNA binding specificity of the PRDM9 protein in human, mice and most other mammals. In budding yeast Saccharomyces cerevisae, which lacks a Prdm9 gene, meiotic breaks are formed opportunistically in the regions of accessible chromatin, primarily at gene promoters. The genome-wide distribution of hotspots in this organism can be altered by tethering Spo11 protein to Gal4 recognition sequences in the strain expressing Spo11 attached to the DNA binding domain of the Gal4 transcription factor. To establish whether similar re-targeting of meiotic breaks can be achieved in PRDM9-containing organisms we have generated a Gal4BD-Spo11 mouse that expresses SPO11 protein joined to the DNA binding domain of yeast Gal4. We have mapped the genome-wide distribution of the recombination initiation sites in the Gal4BD-Spo11 mice. More than two hundred of the hotspots in these mice were novel and were likely defined by Gal4BD, as the Gal4 consensus motif was clustered around the centers in these hotspots. Surprisingly, meiotic DNA breaks in the Gal4BD-Spo11 mice were significantly depleted near the ends of chromosomes. The effect is particularly striking at the pseudoautosomal region of the X and Y chromosomes – normally the hottest region in the genome. Our data suggest that specific, yet-unidentified factors influence the initiation of meiotic recombination at subtelomeric chromosomal regions. Detection of meiotic double strand breaks in mice with a hypomorphic Spo11 allele.

2013-09-11 | E-GEOD-48493 | biostudies-arrayexpress

Genome-wide map of H3K4me3 in 12 day post-partum mouse spermatocytes

Project description:Here we characterize the genome-wide chromatin modification by PRDM9, a histone H3 lysine 4 methyltransferase. In order to detect PRDM9 binding sites we created coisogenic strains of mice differing only in the zinc finger array of PRDM9. One strain is C57BL/6J, which carries the Prdm9Dom2 allele, the other strain was created using genomic replacement and named B6.PRDM9Cst (also called KI), and contains the Prdm9Cst allele originally found in CAST/EiJ mice. Many H3K4me3 positions are common between strains and represent other methyltransferase activity (such as promoters), sites that are unique to one mouse strain likely represent the binding position of that allele of PRDM9.

2014-02-24 | GSE52628 | GEO

Genome-wide identification of PIF1-binding sites and direct-target genes of PIF1 transcriptional regulation in skotomorphogenesis

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF1, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF1 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Three biological replicates data of PIF1-binding sites were collected by comparing the parallel ChIP samples from Myc-epitope-tagged-PIF1 (P1M) overexpressing transgenic seedlings and the wild-type (WT) control.

2014-10-02 | E-GEOD-43283 | biostudies-arrayexpress

Genome-wide identification of PIF4-binding sites and direct-target genes of PIF4 transcriptional regulation in skotomorphogenesis

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF4, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF4 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Three biological replicates data of PIF4-binding sites were collected by comparing the parallel ChIP samples from Myc-epitope-tagged-PIF4 (P1M) overexpressing transgenic seedlings and the wild-type (WT) control.

2014-10-02 | E-GEOD-43284 | biostudies-arrayexpress

Genome-wide maps of FoxP3 binding in transduced CD4+ T cells

Project description:The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability. We used chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) to assess how cofactors affect the genome-wide localization of FoxP3. Chromatin was prepared from primary CD4+ Tconv cells transfected with FLAG-FoxP3 alone or together with GATA1, immunoprecipitated with anti-FLAG, and the bound DNA determined by Illumina deep sequencing. Immunoprecipitation with anti-PolII, or whole cell extract, provided genome-wide controls for transcriptional start sites (TSSd) or for sequencing non-homogeneity, respectively.

2012-08-23 | E-GEOD-40238 | biostudies-arrayexpress

Genome-wide map of transcription factor GATA1 occupancy during mitosis in G1E ER4+E2 cells

Project description:Tissue-specific transcription patterns are preserved throughout cell divisions to maintain lineage fidelity. We investigated whether transcription factor GATA1 plays a role in transmitting hematopoietic gene expression programs through mitosis when transcription is transiently silenced. Live cell imaging revealed that a fraction of GATA1 is retained focally within mitotic chromatin. ChIP-seq of highly purified mitotic cells uncovered that key hematopoietic regulatory genes are occupied by GATA1 in mitosis. The GATA1 co- regulators FOG1 and TAL1 dissociate from mitotic chromatin, suggesting that GATA1 functions as platform for their postmitotic recruitment. Mitotic GATA1 target genes tend to re-activate more rapidly upon entry into G1 than genes from which GATA1 dissociates. A novel system designed to destroy GATA1 specifically during mitosis revealed that mitotic occupancy is required for rapid target gene reactivation. These studies suggest a requirement of mitotic “bookmarking” by GATA1 for the faithful propagation of cell type-specific transcription programs through cell division GATA1 occupancy profiles in mitotic G1E-ER4 +E2 cells generated by ChIP-sequencing. ChIP input DNA was sequenced as control. Previously reported (GSE18164) GATA1 occupancy in asynchrnous G1E-ER4 +E2 cells was analysed and compared with mitotic GATA1 occupancy.

2012-08-17 | E-GEOD-36589 | biostudies-arrayexpress

Genome-wide map of H3K4me3 in HEK293 cells after PRDM9 expression

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