Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression in Aneuploid Drosophila S2 Cells

ABSTRACT: Chromosomal and segmental aneuploidies are usually lethal or common features of cancer cells and variety of disease, but little is known about how copy number relates to gene expression. Drosophila males have a single X chromosome and two sets of autosomes, but X chromosome and autosome transcripts are equally abundant. This 2-fold increase in X chromosome gene expression requires a dosage compensation complex (MSL) that acetylates histone 4 at lysine 16 (H4AcK16). To determine the contribution of general buffering and MSL to X chromosome dosage compensation, we analyzed genome-wide copy number, expression and histone modification pattern in male Drosophila S2 cells with and without MSL. Keywords: Gene Regulation Study, genomic analyses

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE16344 | GEO | 2010/01/11

SECONDARY ACCESSION(S): PRJNA116335

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression in Aneuploid Drosophila S2 Cells

Project description:Chromosomal and segmental aneuploidies are usually lethal or common features of cancer cells and variety of disease, but little is known about how copy number relates to gene expression. Drosophila males have a single X chromosome and two sets of autosomes, but X chromosome and autosome transcripts are equally abundant. This 2-fold increase in X chromosome gene expression requires a dosage compensation complex (MSL) that acetylates histone 4 at lysine 16 (H4AcK16). To determine the contribution of general buffering and MSL to X chromosome dosage compensation, we analyzed genome-wide copy number, expression and histone modification pattern in male Drosophila S2 cells with and without MSL. Keywords: Gene Regulation Study, genomic analyses RNA-seq and microarray were performed in Drosophila non-treated or RNAi treated S2 cells. Two biological replicates were used for expression profile. DNA-seq and CGH were performed (CGH data forthcoming) to check the copy number variation in S2 cells. Chromatin immunoprecipitations were performed in Drosophila non-treated or RNAi treated S2 cells with different histone modification antibodies. At least three biological replicates were performed for each antibody and treatment.

2010-01-11 | E-GEOD-16344 | biostudies-arrayexpress

A sequence motif within chromatin entry sites directs MSL establishment on the Drosophila X chromosome

Project description:Dosage compensation serves as a model for understanding how chromatin-modification enzymes are targeted to initiate and maintain gene regulation. In Drosophila, the MSL complex associates with active genes specifically on the male X chromosome to acetylate histone H4 at lysine 16, and increase expression of most X-linked genes approximately two-fold. To date, no DNA sequence has been discovered to explain the specificity of MSL binding. We previously hypothesized that sequence-specific targeting occurs at initiation or “chromatin entry sites”, but binding to the majority of sites is sequence-independent. Here we characterize more than 150 potential entry sites by ChIP-chip and ChIP-seq and discover a common GA-rich MSL recognition element (MRE). The motif is only slightly enriched on the X chromosome (~2 fold), but this is doubled when considering its preferential location within or 3’ to active X-linked genes (>4 fold enrichment). When inserted on an autosome, a newly identified site can direct local MSL spreading to flanking active genes on the autosome. These results provide strong evidence for both sequence-dependent and -independent steps in MSL targeting of dosage compensation to the male X chromosome.

2008-08-22 | GSE11485 | GEO

MSL complex is attracted to genes marked by H3K36 trimethylation using a sequence-independent mechanism

2007-09-20 | GSE8557 | GEO

Drosophila melanogaster

Project description:Drosophila MSL complex globally acetylates H4 Lys16 on the male X chromosome for dosage compensation

| PRJNA111947 | ENA

Non-coding roX RNAs Prevent the Binding of the MSL-complex to Heterochromatic Regions

Project description:Long non-coding RNAs are involved in dosage compensation both in mammals and in Drosophila by inducing changes in the X-chromosome chromatin structure. In Drosophila melanogaster, roX1 and roX2 are long non-coding RNAs that together with proteins form the male-specific lethal (MSL) complex, which coats the entire male X-chromosome and mediates dosage compensation by increased transcriptional output. It has been shown that in polytene chromosomes, in absence of both roX1 and roX2, the MSL-complex is decreased on the male X-chromosome and found relocated to the chromocenter, and the 4th chromosome. Here we address the role of roX RNAs in MSL-complex targeting and in the evolution of dosage compensation in Drosophila. We performed ChIP-seq experiments and show that MSL-complex recruitment to high affinity sites (HAS) on the X-chromosome is independent on roX and that the HAS sequence motif is conserved in D. simulans. Additionally, a complete and enzymatically active MSL-complex is recruited to six specific genes on the 4th chromosome. Interestingly, our sequence analysis shows that in the absence of roX RNAs, the MSL-complex has affinity to regions enriched in Hoppel transposable elements and to repeats in general. We hypothesize that roX mutants reveal an ancient targeting of the MSL-complex and propose that the role of roX RNAs is to restrict MSL-complex from binding to heterochromatin.

2014-11-07 | GSE58768 | GEO

MSL complex is attracted to genes marked by H3K36 trimethylation using a sequence-independent mechanism

Project description:In Drosophila, X chromosome dosage compensation requires the male-specific lethal (MSL) complex, which associates with actively transcribed genes on the single male X chromosome to upregulate transcription approximately 2-fold. We found that on the male X chromosome, or when MSL complex is ectopically localized to an autosome, histone H3K36 trimethylation (H3K36me3) is a strong predictor of MSL binding. We isolated mutants lacking Set2, the H3K36me3 methyltransferase, and found that Set2 is an essential gene in both sexes of Drosophila. In set2 mutant males, MSL complex maintains X specificity but exhibits reduced binding to target genes. Furthermore, recombinant MSL3 protein preferentially binds nucleosomes marked by H3K36me3 in vitro. Our results support a model in which MSL complex uses high-affinity sites to initially recognize the X chromosome and then associates with many of its targets through sequence-independent features of transcribed genes. Keywords: ChIP-chip ChIP-chip experiments were performed on custom Nimblegen arrays (GPL5636). Each array contained 388,000 oligonucleotide probes covering all of the X and the 2L chromosomes, with a 100 bp resolution (50mer probes with 50 bp gaps). The design was based on FlyBase 3.2. For the superspreading experiments, an additional array was used that contains the entire X chromosome and 3R (GPL5660). MSL complex binding sites on both arrays are the same and signal on the 3R chromosome was at background level.

2007-09-20 | E-GEOD-8557 | biostudies-arrayexpress

Sequence variation within similar cis-elements promotes context-specific functions of two Drosophila GA-binding transcription factors (ChIP-seq data set)

Project description:A key model for understanding how large transcription complexes are targeted is the Drosophila dosage compensation system in which the Male-Specific Lethal (MSL) transcription complex specifically identifies and regulates the male X-chromosome. MSL complex is targeted to GA-containing sequences, but the most well-studied GA-binding transcription factor, GAGA Associated Factor (GAF), does not physically associate with MSL complex. Instead the Chromatin Linked Adapter for MSL Proteins (CLAMP) zinc-finger protein specifically targets MSL complex to GA-rich sequences on the X-chromosome. Here, we compare the binding relationships of CLAMP, GAF, and the MSL3 dosage compensation complex protein using ChIP-seq.

2018-02-01 | GSE107059 | GEO

Chromatin immunoprecipitation of the MSL-1 and MSL-3 vs a mock IP in Drosophila and transcription profiling of X linked genes in WT male or female III instar larvae to provide X chromosome wide profiling of MSL-1 distribution and dosage compensation in Drosophila

Project description:Dosage compensation ensures that males and females, despite unequal number of X chromosomes, equalize for X linked gene expression. In Drosophila, it is achieved by a two-fold up-regulation of most of the genes present on the male X chromosome, and requires the association of the Dosage Compensation Complex (DCC) on the X chromosome. One of the main intriguing aspects of dosage compensation is how this complex is able to target specifically hundreds of sites only on the X chromosome in order to ensure dosage compensation. In order to better understand the targeting of the DCC and the dosage compensation mechanism, we have then decided to analyze the distribution of the DCC as well as the expression levels in male and female in a more complete and precise manner, using microarrays. In this experiment, we present the data used to analyse the distribution of the MSL-1 and MSL-3 protein (part of the DCC complex) on the X chromosome in WT embryos aged from 0H-14H, as well as the distribution of MSL-1 in embryos aged from 4-6H and in male III instar salivary glands. The DNA amplified from the specific immunoprecipitation (MSL-1 or MSL-3 IP) were labelled using Cy5-dCTP and hybridized against DNA amplified from a non specific immunoprecipitation (mock IP), labeled with Cy3 dye. In parralel we present the data used to analyse the expression profile of X-linked genes in WT male or female III instar larvae salivary glands. The cDNA amplified from the RNA extracted from the male or female salivary glands were labelled using Cy5-dUTP and hybridized against the reference sample, labelled with Cy3-dUTP (pool RNA from ON embryos, adultes, and salivary glands mixed at a ratio 1:1:1.and amplified as the RNA from salivary glands). We used for this study a cDNA array developed by the Genecore facility in EMBL, covering the DGC1 and DGC2 cDNA libraries from the Berkeley Drosophila Genome Project, which represents more than 70% of the coding Drosophila genome.

2006-04-01 | E-MEXP-554 | biostudies-arrayexpress

Transcriptome profiling of wild type and Pof mutant Drosophila melanogaster females

Project description:In Drosophila, two chromosome-wide compensatory systems have been characterized; the dosage compensation system acting on the male X-chromosome and the chromosome specific regulation of genes located on the heterochromatic 4th chromosome. Dosage compensation in Drosophila is accomplished by hypertranscription of the single male X-chromosome mediated by the MSL-complex. The mechanism for this compensation is suggested to be an MSL-complex mediated enhanced transcriptional elongation while the mechanism for the compensation mediated by Painting of fourth (POF) on the 4th chromosome has remained elusive. Here we show that POF binds to nascent RNA and this binding is associated with an increase in amount of chromosome 4 transcripts. Furthermore, genes located on the 4th chromosome are enriched in binding of the nucleoplasmic nucleporin component NUP98 and this enrichment correlates to increased POF binding. We also show that genes located in heterochromatic regions have a shorter transition time from site of transcription and to the nuclear envelope. Our current work broadens the understanding about how genes in heterochromatic regions can overcome the repressive influence of their hostile environment.

2012-05-31 | GSE28513 | GEO

Genome-wide profiling of RNA associated to the chromosome 4 specific protein POF in Drosophila melanogaster

2012-05-31 | GSE28518 | GEO

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