Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

21 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A genome-wide RNAi screen draws a genetic framework for transposon control and primary piRNA biogenesis in Drosophila

ABSTRACT: A large fraction of our genome consists of mobile genetic elements. Governing transposons in germ cells is critically important, and failure to do so compromises genome integrity, leading to sterility. In animals, the piRNA pathway is the key to transposon constraint, yet the precise molecular details of how piRNAs are formed and how the pathway represses mobile elements remain poorly understood. In an effort to identify general requirements for transposon control and novel components of the piRNA pathway, we carried out a genome-wide RNAi screen in Drosophila ovarian somatic sheet cells. We identified and validated 87 genes necessary for transposon silencing. Among these were several novel piRNA biogenesis factors. We also found CG3893 (asterix) to be essential for transposon silencing, most likely by contributing to the effector step of transcriptional repression. Asterix loss leads to decreases in H3K9me3 marks on certain transposons but has no effect on piRNA levels. We sequenced small RNAs, RNA-seq and ChIP-seq from either tj-Gal4 driven hpRNA knockdown flies or P-element insertion flies

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Felix Muerdter

PROVIDER: E-GEOD-46009 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

nChIP-seq for CTCF, H3K4me3, H3K27me3 and H3K9me3, in wild type (Hap), STITCH+30kb and STITCH/KRAB clones of human iPS cells.

Project description:We made an insulation (STITCH+30kb) allele of the MYC enhancer in human iPS cells. We integrated a transgene consisting of tetR-KRAB followed by DNA encoding the 2A peptide and the puromycin resistant gene with piggyBac transposition into the genome in the STITCH+30kb clone (STITCH/KRAB). We performed nChIP-seq for CTCF, H3K4me3, H3K27me3 and H3K9me3, in these clones in human iPS cells.

2020-05-01 | E-MTAB-7670 | biostudies-arrayexpress

CapStarr-seq: a high-throughput method for quantitative assessment of enhancer activity in mammals (ChIP-Seq)

Project description:Here we developed CapStarr-Seq, a novel high-throughput strategy to quantitatively assess enhancer activity in mammals. This approach couples capture of regions of interest to previously developed Starr-seq technique. Extensive assessment of CapStarr-seq demonstrated accurate quantification of enhancer activity. Furthermore, we found that enhancer strength correlates with binding complexity of tissue-specific transcription factors and super-enhancers, while additive enhancer activity isolates key genes involved in cell identity and function. ChIP-seq for the transcription factors HEB and TCF1, the DNaseI and the epigenetic modification H3K9me3 in DP thymocytes.

2015-04-09 | E-GEOD-63732 | biostudies-arrayexpress

Epigenetic profiling of well differentiated and dedifferentiated liposarcoma identifies H3K9me3 and Kruppel-like factor 6 (KLF6) as determinants of aggressiveness in sarcoma (ChIP-seq)

Project description:Little is known about the epigenomics of liposarcoma (LPS). Here, we profiled the global expression of 9 epigenetic marks in well differentiated (WD) and dedifferentiated (DD) LPS from 151 patients and found increased H3K9me3 among DDLPS tumors. We performed ChIP-seq and gene expression profiling of patient derived cell lines to discover functionally significant regions of differential H3K9me3 enrichment between WDLPS and DDLPS associated with concomitant gene expression changes. We performed genome-wide transcriptional profiling of H3K9me3 in dedifferentiated liposarcoma DDLPS and well differentiated liposarcoma WDLPS cell lines.

2015-08-04 | E-GEOD-57749 | biostudies-arrayexpress

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [ChIP-seq]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. ChIP-seq with Scl, Hand1, Lsd1, Ezh2, H3K4me1 and H3K27ac in different cell types with mesodermal origin. Scl ChIP-seq in WT, SclKO, SclKO-iScl and Gata12KO mES cell derived day4 EB (embryoid body) Flk1+ mesodermal cells, SclKO-iScl ES cells and MEL cells; Hand1 ChIP-seq in WT mES cell derived day4 EB Flk1+ mesodermal cells; Lsd1 and Ezh2 ChIP-seq in WT and SclKO mES cell derived day4 EB Flk1+ mesodermal cells. ChIP-seq of histone modifications H3K4me1 and H3K27ac in WT, SclKO and Gata12KO mES cell derived day4 EB Flk1+ mesodermal cells, HPC7 hematopoietic progenitor cells and HL1 cardiomyogenic cells

2015-01-01 | E-GEOD-47082 | biostudies-arrayexpress

ChIP-seq data of Epstein-Barr Virus Nuclear Antigen Leader ProteinM-BM- (EBNALP)

Project description:Epstein-Barr-Virus (EBV) Nuclear Antigens EBNALP and EBNA2 are co-expressed in EBV infected B-lymphocytes and are critical for Lymphoblastoid Cell Line (LCL) growth. EBNALP removes NCOR1 and RBPJ repressive complexes from promoter and enhancer sites and EBNA2 mostly activates transcription from distal enhancers. ChIP-seqs found EBNALP at 19,224 LCL sites, which were 33% promoter associated. EBNALP was associated with 10 transcription factor (TF) clusters that included YY1(63%), SP1(62%), PAX5(59%), BATF(50%), IRF4(49%), RBPJ(43%), ETS1(39%), PU.1(37%), RAD21(33%), NF-kB(31%), TBLR1(26%), ZNF143(24%), CTCF(23%), SMC3(21%), and EBF(17%). EBNALP sites had higher H3K4me3, H3K9ac, H3K27ac, H2Az, and RNA Pol II signals than EBNA2 sites and had similar transcription effects. EBNALP co-localized with 29% of 19,845 EBNA2 sites. EBNALP/EBNA2 sites were similar to EBNALP sites in promoter localization, associated cell TFs, Pol II, H3K4me3, H3K9ac, H3K27ac, and H2Az signals. EBNALP and EBNA2 promoter sites were more transcriptionally active than EBNALP or EBNA2 promoter sites. EBNALP was at the enhancer or promoter of myc and MYC affected genes, including cyclin D2, and bcl2. EBNALP at promoters with DNA looping and transcription factors, is positioned to deplete repressors from enhancers and promoters, enable chromatin remodeling, and transcription activation. Two EBNALP ChIP-seq replicates from IB4 LCL are analyzed in this study.

2013-07-31 | E-GEOD-49338 | biostudies-arrayexpress

Comprehensive Epigenomic Analysis Reveals Dynamic Regulatory Programs Of Blood Development (ChIP-seq)

Project description:Embryonic hematopoiesis is regulated by the coordinated interaction between transcription factors and the epigenetic regulators driving developmental-stage specific gene expression but how this process drives hematopoietic specification and terminal differentiation is poorly understood. Here we generated RNA-Seq, DNase-Seq and ChIP-Seq data for histone marks and transcription factors from ES-cell derived purified cells representing six sequential stages of blood cell specification and differentiation. Our data reveal the binding patterns of specific transcription factors involved in the priming and maintenance of distal elements and inform how binding impacts on promoter activity. Functional studies based on these data uncovered a previously unrecognised role for Hippo signalling in mammalian hematopoietic specification. Finally, we present a dynamic core regulatory network model for hematopoiesis and demonstrate its utility for the design of reprogramming experiments. Our study represents a powerful resource for studying hematopoiesis and demonstrates how such data can advance our understanding of mammalian development. ChIP-seq data of histone modifications and transcription factors, and RNA-seq data obtained from purified cells representing five sequential stages of murine blood cell specification and differentiation

2016-02-26 | E-GEOD-69096 | biostudies-arrayexpress

Physiological Vascular Permeability Requires Induction of Endothelial NR4A1 by Progesterone Receptor [ChIP-Seq]

Project description:Vascular permeability is frequently associated with inflammation and it is triggered by chemokines and by a cohort of secreted permeability factors, such as VEGF. In contrast, here we showed that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and it is independent of VEGF. Both global and endothelial-specific deletion of PR block physiological vascular permeability in the uterus while misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of genome-wide transcriptional profile of endothelium and ChIP-sequencing revealed that PR induces a NR4A1 (Nur77/TR3) specific transcriptional program that broadly regulates vascular permeability in response to progesterone. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely and venule-specific regulation of vascular barrier function. Silencing NR4A1 blocks PR-mediated permeability responses indicating a direct link between PR and NR4A1. These results reveal a previously unknown function for progesterone receptor on endothelial cell biology with consequences to physiological vascular permeability and implications to the clinical use of progestins and anti-progestins on blood vessel integrity. Examination of PR binding sites in HUVEC cells using ChIP-seq (non-infected-negative control, PR infected followed by ligand treatment-PR+P or vehicle PR)

2014-01-01 | E-GEOD-43786 | biostudies-arrayexpress

Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation [ChIP-seq]

Project description:The histone 3 lysine 9 (H3K9)-specific methyltransferase (KMT) Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on Setdb1 role(s) in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for muscle adult stem cells expansion following activation and in vitro studies on skeletal myoblasts confirmed that Setdb1 suppresses terminal myoblast differentiation. We used genome-wide analyses to identify Setdb1 direct target genes in myoblasts and observed a release of Setdb1 from the promoter of selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. We demonstrated that both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Taken together, our findings uncover a functional link between Setdb1 and canonical Wnt signalling in skeletal muscle cells, which affects the expression of a subset of Setdb1 target genes. We revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions. ChIP-seq of Setdb1 and H3K9me3 in Myoblast cells (C2C12)

2016-02-01 | E-GEOD-65493 | biostudies-arrayexpress

Notch1-driven epigenetic changes in a mouse model of T cell Acute Lymphoblastic Leukemia (T-ALL)

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we used a mouse model of T-ALL through the overexpression of the intarcellular transcriptionally active part of Notch1 (N1-IC). This model faithfully recapitulates the major characteristics of the human disease. Comparison of the leukemic cells from peripheral tumors(thymoma) of this mouse model to normal thymic cells Double Positive (DP) for the markers CD4 and CD8 that express very low levels of Notch1 showed major expression changes (please see GSE34554) in pathways controlling the transition from physiology to disease. Further correlation of the data to ChIP-Seq data from the same cell populations led us to identify a hitherto unknown antagonism of the Notch1 oncogenic pathway and the polycomb complex (PRC2) in leukemia. Importantly exome sequencing in primary samples from human patients with T-ALL revealed that the PRC2 complex is frequently mutated and inactivated, further supporting the tumor suppressor role of the complex in this disease. Gene expression profiles from CD4+/8+ Double Positive (named DP) derived from normal thymus and Notch1-IC over-expressing tumors (named T-ALL) were analyzed for the genomewide enrichments of two major activating epigenetic marks (Histone 3 Lysine 9 acetylation (H3K9ac) and lysine 4 trimethylation (H3K4me3)), one reprressive mark (Histone 3 lysine 27 trimethylation, H3K27me3) and the major oncogene Notch1.

2012-01-10 | E-GEOD-34954 | biostudies-arrayexpress

Dissecting the dynamic changes of 5-hydroxymethylcytosine in T cell development and differentiation [ChIP-Seq]

Project description:The discovery of TET proteins, enzymes that oxidize 5-methylcytosine (5mC) in DNA, has revealed novel mechanisms for the regulation of DNA methylation. We have mapped 5-hydroxymethylcytosine (5hmC) at different stages of T cell development in the thymus and T cell differentiation in the periphery. We show that 5hmC is enriched in the gene body of highly expressed genes at all developmental stages, and that its presence correlates positively with gene expression. Further emphasizing the connection with gene expression, we find that 5hmC is enriched in active thymus-specific enhancers, and that genes encoding key transcriptional regulators display high intragenic 5hmC levels in precursor cells at those developmental stages where they exert a positive effect. Our data constitute a valuable resource that will facilitate detailed analysis of the role of 5hmC in T cell development and differentiation. Examine the distribution of the H3K27Ac in DP T cells. The presence of H3K27Ac in enhancers enable us to distinguish poised(H3Kme1 enriched, but devoid of H3K27Ac) versus active enhancers (enriched for H3K4me1 and H3K27Ac).

2014-08-04 | E-GEOD-59117 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data