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Expansion of GA dinucleotide repeats increases the density of CLAMP binding sites on the X-chromosome to promote Drosophila dosage compensation [ChIP-Seq]

ABSTRACT: Expansion of GA dinucleotide repeats increases the density of CLAMP binding sites on the X-chromosome to promote Drosophila dosage compensation [ChIP-Seq]

PROVIDER: PRJNA325925 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3675040.fastq.gz	Fastqsanger.gz
	SRR3675041.fastq.gz	Fastqsanger.gz
	SRR3675042.fastq.gz	Fastqsanger.gz
	SRR3675043.fastq.gz	Fastqsanger.gz
	SRR3675044.fastq.gz	Fastqsanger.gz

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Similar Datasets

Expansion of GA dinucleotide repeats increases the density of CLAMP binding sites on the X-chromosome to promote Drosophila dosage compensation

Project description:Expansion of GA dinucleotide repeats increases the density of CLAMP binding sites on the X-chromosome to promote Drosophila dosage compensation

| PRJNA325937 | ENA

Expansion of GA dinucleotide repeats increases the density of CLAMP binding sites on the X-chromosome to promote Drosophila dosage compensation [ChIP-Seq]

Project description:ChIP-seq was performed to compare binding the genome-wide binding profile of the CLAMP transcription factor in two different Drosophila species. ChIP seq experiments compare the binding profile of CLAMP in female larvae to identify conservation of its binding sequence.

2016-07-17 | E-GEOD-83435 | biostudies-arrayexpress

Expansion of GA dinucleotide repeats increases the density of CLAMP binding sites on the X-chromosome to promote Drosophila dosage compensation [ChIP-Seq]

Project description:ChIP-seq was performed to compare binding the genome-wide binding profile of the CLAMP transcription factor in two different Drosophila species.

2016-07-17 | GSE83435 | GEO

The interaction of MLE with CLAMP zinc finger domains is important for dosage compensation in Drosophila melanogaster

Project description:The Drosophila male-specific lethal (MSL) complex binds to the male X chromosome to activate transcription, and consists of five proteins, MSL1, MSL2, MSL3, MOF, MLE, and two roX RNAs. The MLE helicase remodels the roX lncRNAs, enabling the lncRNA-mediated assembly of the Drosophila dosage compensation complex. MSL2 is expressed only in males and interacts with the N-terminal zinc-finger of the transcription factor CLAMP that is important for specific recruitment of the MSL complex on the male X chromosome. Here we found that the unstructured C-terminal region of MLE interacts with 6-7 zinc-finger domains of CLAMP. In vitro 4-5 zinc fingers are critical for specific DNA-binding of CLAMP with GA-repeats, which constitute the core motif at the high affinity binding sites for MSL proteins. Deletion of the Clamp Binding Domain (CBD) in MLE results in decreasing of MSL proteins association with male X chromosome and increasing of male lethality. These results suggest that interactions of unstructured regions in MSL2 and MLE with CLAMP zinc finger domains are important for the specific recruitment of the MSL complex on the male X chromosome.

2024-03-20 | GSE239354 | GEO

Synergistic interactions between CLAMP and MSL complex facilitate Drosophila dosage compensation

Project description:ChIP-seq and mRNA-seq experiments were performed to understand the role of the CLAMP protein in dosage compensation ChIP-seq experiments compared the binding profiles of CLAMP in male and female cells and mRNA-seq data to define the role of CLAMP in regulating genes on the X-chromosome

2013-07-15 | E-GEOD-39271 | biostudies-arrayexpress

Histone locus regulation by the Drosophila dosage compensation adaptor protein CLAMP

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 zinc-finger protein binds these GA-repeat motifs, increases chromatin accessibility, enhances histone gene transcription, and promotes HLB formation. We previously demonstrated 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.

2017-11-15 | GSE102922 | GEO

Histone locus regulation by the Drosophila dosage compensation adaptor protein CLAMP

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

Synergistic interactions between CLAMP and MSL complex facilitate Drosophila dosage compensation

Project description:ChIP-seq and mRNA-seq experiments were performed to understand the role of the CLAMP protein in dosage compensation

2013-07-15 | GSE39271 | GEO

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

Expansion of GA Dinucleotide Repeats Increases the Density of CLAMP Binding Sites on the X-Chromosome to Promote Drosophila Dosage Compensation.

Project description:Dosage compensation is an essential process that equalizes transcript levels of X-linked genes between sexes by forming a domain of coordinated gene expression. Throughout the evolution of Diptera, many different X-chromosomes acquired the ability to be dosage compensated. Once each newly evolved X-chromosome is targeted for dosage compensation in XY males, its active genes are upregulated two-fold to equalize gene expression with XX females. In Drosophila melanogaster, the CLAMP zinc finger protein links the dosage compensation complex to the X-chromosome. However, the mechanism for X-chromosome identification has remained unknown. Here, we combine biochemical, genomic and evolutionary approaches to reveal that expansion of GA-dinucleotide repeats likely accumulated on the X-chromosome over evolutionary time to increase the density of CLAMP binding sites, thereby driving the evolution of dosage compensation. Overall, we present new insight into how subtle changes in genomic architecture, such as expansions of a simple sequence repeat, promote the evolution of coordinated gene expression.

| S-EPMC4945028 | biostudies-literature

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