Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptionally Driven DNA Replication Programme of the Human Parasite Leishmania major

ABSTRACT: Faithful inheritance of the large eukaryotic genomes requires the orchestrated activation of multiple DNA replication origins. Although origin activation is mechanistically conserved among eukaryotes, how replication origins are specified and selected for activation in each S-phase seem to differ across the model systems studied. Here we provide a complete analysis of the nucleosomal landscape and replication programme of the human parasite Leishmania major, building on a better evolutionary understanding of replication organization in Eukarya. We found that active transcription is a driving force for the nucleosomal organization of L. major genome, and that both the spatial and the temporal programme of DNA replication can be explained as associated to RNA polymerase kinetics, without the need to invoke specific regulatory mechanisms. This simple scenario likely provides these organisms with the flexibility and robustness to deal with the continuous environmental changes that impose alterations in their genetic programmes during their parasitic life cycle stages. Our findings also suggest that coupling replication initiation to transcription elongation could be an ancient solution used by eukaryotic cells for origin maintenance Replication intitiation sites were defined using two replicates of short nascent strands of increasing sizes (F4 and F5) purified through three rounds of Lambda-exonuclease digestion, and a genomic DNA control (Ctrl). Nucleosome landscape was determined using two replicates of mononucleosomal-DNA derived from MNase-digested chromatin

ORGANISM(S): Leishmania major strain Friedlin

SUBMITTER: Maria Gomez

PROVIDER: E-GEOD-81991 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Tissue-specific regulation of chromatin insulator function

Project description:Chromatin insulators organize the genome into distinct transcriptional domains and contribute to cell type-specific chromatin organization. However, factors regulating tissue-specific insulator function have not yet been discovered. Here we identify the RNA recognition motif-containing protein, Shep, as a direct interactor of two individual components of the gypsy insulator complex in Drosophila. Mutation of shep improves gypsy-dependent enhancer blocking, indicating a role as a negative regulator of insulator activity. Unlike ubiquitously expressed core gypsy insulator proteins, Shep is highly expressed in the central nervous system (CNS) with lower expression in other tissues. We developed a novel, quantitative tissue-specific barrier assay to demonstrate that Shep functions as a negative regulator of insulator activity in the CNS but not in muscle tissue. Additionally, mutation of shep alters insulator complex nuclear localization in the CNS but not other tissues. Consistent with negative regulatory activity, ChIP-seq analysis of Shep in a CNS-derived cell line indicates substantial genome-wide colocalization with a single gypsy insulator component but limited overlap with intact insulator complexes. Taken together, these data reveal a novel, tissue-specific mode of regulation of a chromatin insulator. ChIP-seq of Shep, Su(Hw), and Mod(mdg4)2.2 in Drosophila BG3 cells along with alternate antibodies

2012-11-30 | E-GEOD-40797 | biostudies-arrayexpress

The activation of IL-1 induced enhancers depends on TAK1 kinase activity and NF-KB p65 [ChIP-Seq]

Project description:The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-κB subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-κB p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-κB-dependent enhancers in epithelial cells. ChIP-seq in KB cells with 5 different antibodies under different treatment conditions

2014-12-16 | E-GEOD-64223 | biostudies-arrayexpress

Enrichment of processed pseudogene transcripts in L1-ribonucleoprotein particles

Project description:We explored the RNA binding properties of LINE-1 ORF1p, both free and in the L1 RNP, using a recently developed photoactivatable-ribonucleoside-enhanced crosslinking and immunoprecipitation technique (PAR-CLIP) to comprehensively identify ORF1p binding sites in the transcriptome of human cells (HEK293T). Our results show that ORF1p binds to a wide range of cellular mRNAs, with an enrichment for binding at the 3’ UTR. Our data also show that ORF1p binds very strongly with retrotransposable RNA, i.e., L1, Alu and SVA. PAR-CLIP analysis of L1 RNPs and free ORF1p RNA binding profiles, comparison to HuR RNA binding profile

2013-05-21 | E-GEOD-43801 | 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

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [RRBS]

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. Examination of Scl and Gata 1 & 2 target genes in ES cell derived day4.75 EB (embryoid body) Tie2+CD31+CD41- endothelial cells

2015-01-01 | E-GEOD-56359 | biostudies-arrayexpress

Histone H3 Lysine4 Acetylation-Methylation Dynamics Define Breast Cancer Subtypes [ChIP-seq]

Project description:The molecular signature at histone H3K4 involved in epigenetic regulation of normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology. This study examines the dynamic distribution of H3K4me3 and H3K4ac histone modification associated with active chromatin to provide an understanding of the changes in epigenetic regulation associated with the unique breast cancer subtypes. H3K4me3 and H3K4ac histone modification study in normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology

2016-02-10 | E-GEOD-69377 | biostudies-arrayexpress

Genome-wide identification of Ikaros binding sites in pre-B cells

Project description:Ikaros DNA binding proteins are important regulators of haematopoiesis and genetic deletion of Ikaros results in severe developmental disturbances, including delayed thymocyte differentiation and an early and complete block in B cell development. Although Ikaros ChIP-seq data are available for mouse thymocytes and human haematopoietic progenitors, it has not been achieved in B cell progenitors. The goal of this study was to identify Ikaros binding sites in pre-B cells to define Ikaros target genes which could explain the essential role of Ikaros proteins in B cell differentiation. We carried out chromatin immunoprecipitation and high throughput sequencing (ChIP-seq) with antibodies to the C-terminus of endogenous Ikaros in B3 cells and with anti-haemagglutinin (HA) in B3 cells transduced with epitope-tagged HA-Ikaros.

2013-01-15 | E-GEOD-38169 | biostudies-arrayexpress

ChIP-seq of circadian transcription factors in MLL-AF9 leukemia cell lines

Project description:We performed ChIP-seq of two core circadian TFs which were found to be important in leukemia proliferation, in order to identify potential target genes regulated by the circadian rhythm. Here, we performed ChIP-seq for the core circadian transcription factors CLOCK and ARNTL (BMAL1) in NOMO-1 and THP-1 cells.

2016-07-03 | E-GEOD-70686 | biostudies-arrayexpress

BRACHYURY orchestrates distinct mesoderm and endoderm gene regulatory networks in differentiating human embryonic stem cells

Project description:The transcription factor BRACHYURY (T, BRA) is one of the first markers of gastrulation and lineage specification in mammals. Despite its wide use and importance in stem cell and developmental biology, its genomic targets are largely unknown. Here, we used differentiated human embryonic stem cells to study the role of BRA in Bmp4-induced mesoderm and Activin-induced endoderm progenitors by ChIP-seq. We show that BRA has distinct genome-wide binding landscapes in these two populations. Our data illuminate the function of BRA in the context of human embryonic development and show that the regulatory role of BRA is context-dependent. ChIP-seq of BRACHYURY (T, BRA) in two cell types: endoderm and mesoderm progenitors derived from human embryonic stem cells after 36 hours of growth in chemically-defined media (described in Bernardo et al., Cell Stem Cell, 2011, 9:144-155). Input DNA samples are included as a control.

2015-05-18 | E-GEOD-60606 | biostudies-arrayexpress

Comprehensive Epigenomic Analysis Reveals Dynamic Regulatory Programs Of Blood Development (TF 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-69099 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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