Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

70 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromosomal High Affinity Binding Sites for the Drosophila Dosage Compensation Complex.

ABSTRACT: We identified 131 high affinity sites of the Drosophila DCC combining residual ChIP-chip profiles after differential crosslinking and RNAi-mediated knockdown of spreading factors Keywords: ChIP-chip MSL1 and MSL2 ChIP under various conditions including differential crosslinking and RNAi against MOF, MLE and MSL3. 2-4 replicates per experiment. dye-swaps as indicated in sample description.

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Tobias Straub

PROVIDER: E-GEOD-12292 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

The chromosomal high-affinity binding sites for the Drosophila dosage compensation complex.

Straub Tobias T Grimaud Charlotte C Gilfillan Gregor D GD Mitterweger Angelika A Becker Peter B PB

PLoS genetics 20081212 12

Dosage compensation in male Drosophila relies on the X chromosome-specific recruitment of a chromatin-modifying machinery, the dosage compensation complex (DCC). The principles that assure selective targeting of the DCC are unknown. According to a prevalent model, X chromosome targeting is initiated by recruitment of the DCC core components, MSL1 and MSL2, to a limited number of so-called "high-affinity sites" (HAS). Only very few such sites are known at the DNA sequence level, which has preclud ...[more]

PMID: 19079572

Similar Datasets

JIL kinase – marker of active chromatin and sensor of dosage compensation

Project description:ChIP-chip profiles of JIL-1, H3S10phK14ac and H4K16ac in Drosophila S2 cells JIL-1, H3S10phK14ac and H4K16ac ChIP in Drosophila S2 cells. 2-4 biological replicates per experiment. dye-swaps as indicated in sample description

2011-02-01 | E-GEOD-22618 | biostudies-arrayexpress

ChIP-chip profiles of MLE, MSL3 and MOF in Drosophila S2 cells

Project description:ChIP-chip profiles of MLE, MSL3 and MOF in Drosophila S2 cells MLE, MSL3 amd MOF ChIP in Drosophila S2 cells. 1-5 biological replicates per experiment. dye-swaps as indicated in sample description

2012-12-11 | E-GEOD-37863 | biostudies-arrayexpress

Differential Chromatin Binding of the Drosophila Dosage Compensation Complex

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

2012-12-11 | E-GEOD-37865 | biostudies-arrayexpress

Chromosomal kinase JIL-1 in Drosophila S2 Cells

Project description:This SuperSeries is composed of the following subset Series: GSE22618: JIL kinase – marker of active chromatin and sensor of dosage compensation GSE22620: JIL-1 RNAi in Drosophila S2 Cells Refer to individual Series

2011-02-01 | E-GEOD-22621 | biostudies-arrayexpress

JIL kinase - marker of active chromatin and sensor of dosage compensation

Project description:ChIP-chip profiles of RNA Polymerase II phosphorylated on serine 2 in Drosophila S2 cells. RNA Polymerase II phosphorylated on serine 2 ChIP in Drosophila S2 cells. 3 biological replicates with dye-swaps.

2012-05-07 | E-GEOD-37784 | biostudies-arrayexpress

Analysis of genome-wide binding of the insulator factors CTCF and CP190

Project description:We identified about 3000 CTCF sites in the genome. In addition to binding to CTCF sites we found CP190 to bind to transcriptional start sites of actively transcribed genes where it inversely correlates with nucleosome occupancy. Keywords: ChIP-chip CTCF and CP190 ChIP. 2 biological replicates per experiment. dye-swaps as indicated in sample description.

2010-05-05 | E-GEOD-12749 | biostudies-arrayexpress

The activation potential of MOF is constrained for dosage compensation

Project description:The H4K16 acetyltransferase MOF plays a crucial role in dosage compensation in Drosophila, but has additional, global functions. We compared the molecular context and effect of MOF in male and female flies combining chromosome-wide mapping and transcriptome studies with analyses of defined reporter loci in transgenic flies. MOF distributes dynamically between two complexes, the Dosage Compensation Complex and a complex containing MBD-R2, a global facilitator of transcription. These different targeting principles define the distribution of MOF between the X chromosome and autosomes and at transcription units with 5’ or 3’ enrichment. The male X chromosome differs from all other chromosomes in that H4K16 acetylation levels do not correlate with transcription output. The reconstitution of this phenomenon at a model locus revealed that the activation potential of MOF is constraint in male cells in the context of the DCC to arrive at the two-fold activation of transcription characteristic of dosage compensation. ChIP-chip profiling of MBD-R2, MOF and MSL1 in adult male and female flies, and SL2 cells, incl. at least 3 biological replicates

2010-06-26 | E-GEOD-20695 | biostudies-arrayexpress

ChIP-seq mapping of histone modifications in CD14++ CD16- monocytes from septic disease patients

Project description:Chromatin immunoprecipitation with antibodies specific for histone modifications H3K4me3, H3K9ac and H3K27me3 and subsequent high-throughput sequencing were performed on fixed chromatin from two septic disease patients. ChIP-seq

2015-03-01 | E-GEOD-62908 | biostudies-arrayexpress

ChIP-seq mapping of histone modifications in CD14++ CD16- monocytes from human blood samples

Project description:Chromatin immunoprecipitation in combination with a genome-wide analysis via high-throughput sequencing is the state of the art method to gain genome-wide representation of histone modification or transcription factor binding profiles. However, chromatin immunoprecipitation analysis in the context of human experimental samples is limited, especially in the case of blood cells. The typically extremely low yields of precipitated DNA are usually not compatible with library amplification for next generation sequencing. We developed a highly reproducible protocol to present a guideline from the first step of isolating monocytes from a blood sample to analyse the distribution of histone modifications in a genome-wide manner. ChIP-seq histone modifications in CD14++ CD16- monocytes from human blood samples

2014-09-01 | E-GEOD-54634 | biostudies-arrayexpress

Genome-wide DNA-binding profile of HNF4A and genome occupancy of the histone modifications H3K4me1, H3K27ac in kidneys from Bicc1 WT and KO mice by ChIPseq.

Project description:Mutations in Bicaudaul C 1 (BICC1), evolutionary conserved RNA-binding protein, cause renal cysts in mice and humans. These renal cysts are reminiscent of Polycystic Kidney Disease (PKD). How BICC1 is involved in the pathogenesis of polycystic kidney disease is still unknown. Recent studies highlighted that HNF4A plays a role in the regulation of metabolic pathways deregulated in this renal disease. Moreover, Menezes et al. [2012, https://doi.org/10.1371/journal.pgen.1003053] showed that combined kidney inactivation of Hnf4a and Pkd1 in mice significantly worsened the cystic phenotype. Here we investigated whether the DNA binding and transcriptional activity of HNF4A might be deregulated in kidneys from Bicc1 mouse model of polycystic kidney disease. HNF4A, H3K27ac, H3K4me1 ChIPseq experiments were performed in kidneys from male and female Bicc1 WT and KO mice. From the contralateral kidneys of the same animals used for the ChIPseq experiments, the total RNA was extracted for gene expression profiling by RNAseq. The RNAseq data was used to support the ChIP-seq analysis and to reveal deregulated pathways in BICC1 mutants.

2020-01-20 | E-MTAB-6424 | 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