Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA399285 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5952580_1.fastq.gz | Fastqsanger.gz | |||
| SRR5952580_2.fastq.gz | Fastqsanger.gz | |||
| SRR5952581_1.fastq.gz | Fastqsanger.gz | |||
| SRR5952581_2.fastq.gz | Fastqsanger.gz | |||
| SRR5952582_1.fastq.gz | Fastqsanger.gz |
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Project description:Histone locus regulation by the Drosophila dosage compensation adaptor protein CLAMP
| PRJNA489269 | ENA
Project description:The essential process of dosage compensation, which corrects for the imbalance in X-linked gene expression between XX females and XY males, represents a key model for how genes are targeted for coordinated regulation. However, the mechanism by which dosage compensation complexes identify the X-chromosome during early development remained unknown because of the difficulty of sexing embryos prior to zygotic transcription. We used meiotic drive to sex Drosophila embryos prior to zygotic transcription and ChIP-seq to measure dynamics of dosage compensation factor targeting. The Drosophila Male-Specific Lethal dosage compensation complex (MSLc) requires the ubiquitous zinc-finger protein Chromatin-Linked Adaptor for MSL Proteins (CLAMP) to identify the X-chromosome. We observe a multi-stage process in which MSLc first identifies CLAMP binding sites throughout the genome followed by concentration at the strongest X-linked MSLc sites. We provide insight into the dynamic mechanism by which a large transcription complex identifies its binding sites during early development.
2019-12-01 | GSE133637 | GEO
Project description:Synergistic interactions between CLAMP and MSL complex facilitate Drosophila dosage compensation
| PRJNA170445 | ENA
Project description:The conserved histone locus body (HLB) assembles prior to zygotic gene activation early during development and concentrates factors into a nuclear domain of coordinated histone gene regulation. Although HLBs form specifically at replication-dependent histone loci, the cis and trans factors that target HLB components to histone genes remained unknown. Here we report that conserved GA repeat cis elements within the bidirectional histone3-histone4 promoter direct HLB formation in Drosophila In addition, the CLAMP (chromatin-linked adaptor for male-specific lethal [MSL] proteins) zinc finger protein binds these GA repeat motifs, increases chromatin accessibility, enhances histone gene transcription, and promotes HLB formation. We demonstrated previously that CLAMP also promotes the formation of another domain of coordinated gene regulation: the dosage-compensated male X chromosome. Therefore, CLAMP binding to GA repeat motifs promotes the formation of two distinct domains of coordinated gene activation located at different places in the genome.
2018-09-05 | GSE119448 | GEO
Project description:The essential process of dosage compensation is required to equalize gene expression of X-chromosome genes between males (XY) and females (XX). In Drosophila, the conserved Male-specific lethal (MSL) histone acetyltransferase complex mediates dosage compensation by increasing transcript levels from genes on the single male X-chromosome approximately two-fold. Consistent with its increased levels of transcription, the male X-chromosome has enhanced chromatin accessibility, distinguishing it from the autosomes. Here, we demonstrate that the non-sex specific CLAMP (Chromatin-linked adaptor for MSL proteins) zinc finger protein that recognizes GA-rich sequences genome-wide promotes the specialized chromatin environment on the male X-chromosome. In contrast, MSL complex is not required for global male X-chromosome chromatin accessibility, and instead promotes chromatin accessibility just at its highest-occupancy sites. Overall, our results support a model where synergy between the global increases in accessibility promoted by CLAMP and the local effects of MSL complex create a specialized chromatin domain on the male X-chromosome.
2017-10-31 | GSE99893 | GEO
Project description:The essential process of dosage compensation is required to equalize gene expression of X-chromosome genes between males (XY) and females (XX). In Drosophila, the conserved Male-specific lethal (MSL) histone acetyltransferase complex mediates dosage compensation by increasing transcript levels from genes on the single male X-chromosome approximately two-fold. Consistent with its increased levels of transcription, the male X-chromosome has enhanced chromatin accessibility, distinguishing it from the autosomes. Here, we demonstrate that the non-sex specific CLAMP (Chromatin-linked adaptor for MSL proteins) zinc finger protein that recognizes GA-rich sequences genome-wide promotes the specialized chromatin environment on the male X-chromosome. In contrast, MSL complex is not required for global male X-chromosome chromatin accessibility, and instead promotes chromatin accessibility just at its highest-occupancy sites. Overall, our results support a model where synergy between the global increases in accessibility promoted by CLAMP and the local effects of MSL complex create a specialized chromatin domain on the male X-chromosome.
2017-10-31 | GSE99842 | GEO
Project description:Drosophila X chromosomes are subject to dosage compensation in males and are known to have a specialized chromatin structure in the male soma. We are interested in how specific chromatin structure change contributes to X chromosome hyperactivity and dosage compensation. We have conducted a global analysis of localize two dosage compensation complex dependent histone marks H4AcK16 and H3PS10 and one dosage compensation complex independent histone mark H3diMeK4 in the genome, especially on X chromosome by ChIP-chip approach in both male and female adult flies. We also probed general genomewide chromatin structure by deep DNA sequencing of sheared ChIP input DNA from male and female adult flies.
2010-01-11 | GSE15593 | GEO
Project description:Drosophila X chromosomes are subject to dosage compensation in males and are known to have a specialized chromatin structure in the male soma. We are interested in how specific chromatin structure change contributes to X chromosome hyperactivity and dosage compensation. We have conducted a global analysis of localize two dosage compensation complex dependent histone marks H4AcK16 and H3PS10 and one dosage compensation complex independent histone mark H3diMeK4 in the genome, especially on X chromosome by ChIP-chip approach in both male and female adult flies. We also probed general genomewide chromatin structure by deep DNA sequencing of sheared ChIP input DNA from male and female adult flies. Chromatin immunoprecipitations were performed in 5-7 day aged adult male and female flies with three histone modification antibodies. ChIP enriched DNA and input DNA was labeled by Cy3 or Cy5 dye separately and hybridized simultaneously to the Drosophila FlyGEM arrays. At least two biological replicates were performed for each antibody and sex. DNA-seq (NIDDK-Drosophila-Illumina-DNASeq) were performed on ChIP-input sheared DNA to check the general chromatin structure of different chromosome.
2010-01-11 | E-GEOD-15593 | biostudies-arrayexpress
Project description:Transcription regulators select their genomic binding sites from a large pool of similar, non‑functional sequences. Although general principles that allow such discrimination are known, the complexity of DNA elements often precludes a prediction of functional sites. The process of dosage compensation in Drosophila allows exploring the rules underlying binding site selectivity. The male-specific-lethal (MSL) Dosage Compensation Complex selectively binds to some 300 X-chromosomal ‘High Affinity Sites’ (HAS) containing GA‑rich ‘MSL recognition elements’ (MREs), but disregards thousands of other MRE sequences in the genome. The DNA‑binding subunit MSL2 alone identifies a subset of MREs, but fails to recognize most MREs within HAS. The ‘Chromatin-linked adaptor for MSL proteins’ (CLAMP) also interacts with many MREs genome‑wide and promotes DCC binding to HAS. Using genome‑wide DNA‑immunoprecipitation we describe extensive cooperativity between both factors, depending on the nature of the binding sites. These are explained by physical interaction between MSL2 and CLAMP. In vivo, both factors cooperate to compete with nucleosome formation at HAS. The male‑specific MSL2 thus synergises with a ubiquitous GA‑repeat binding protein for refined X/autosome discrimination.
2018-12-05 | GSE119708 | GEO
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