Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Factor cooperation for chromosome discrimination in Drosophila

ABSTRACT: Factor cooperation for chromosome discrimination in Drosophila

PROVIDER: PRJNA490090 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7813050_1.fastq.gz	Fastqsanger.gz
	SRR7813050_2.fastq.gz	Fastqsanger.gz
	SRR7813060_1.fastq.gz	Fastqsanger.gz
	SRR7813060_2.fastq.gz	Fastqsanger.gz
	SRR7813070.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 91

Similar Datasets

Factor cooperation for chromosome discrimination in Drosophila

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

Factor cooperation for chromosome discrimination in Drosophila.

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 (DCC) 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.

| S-EPMC6393291 | biostudies-literature

Pioneer and nonpioneer factor cooperation drives lineage specific chromatin opening

Project description:Pioneer and nonpioneer factor cooperation drives lineage specific chromatin opening

| PRJNA517135 | ENA

Drosophila melanogaster 2nd chromosome substitution lines

Project description:Transcriptional profiling of Drosophila melanogaster 2nd chromosome substitution lines; Background chromosomes are identical across lines; 2nd chromosomes are different across line and can be homozygous or heterozygous within each line Keywords: Natural variation

2010-05-06 | GSE12191 | GEO

Transcription factor cooperation and competition

Project description:Transcription factors have to distinguish proper targets from a large pool of potential binding sites. Here we explore how MSL2 and CLAMP cooperate to bind their specific targets. Using an in vitro chromatin reconstitution system and by mutating the interaction domain of CLAMP we show how direct and indirect cooperation of TF binding influence binding specificity.

2023-07-27 | GSE224981 | GEO

Gene expression variation in Y-chromosome substitution lines of Drosophila melanogaster

Project description:These arrays were done in the context of a study to probe gene expression variation across Y-chromosome substitution lines of Drosophila melanogaster Keywords: polymorphism, evolution, chromosome substitution

2008-04-30 | GSE9457 | GEO

Mitochondrial - Y Chromosome Epistasis in Drosophila melanogaster

Project description:We generate 36 otherwise isogenic Drosophila melanogaster strains differing only in the geographical origin of their mitochondrial genome and Y chromosome to experimentally examine the effects of the uniparentaly inherited parts of the genome, as well as their interaction, in males. We assay gene expression through RNA-sequencing and detect an important role for both mitochondrial and Y-linked genes, as well as extensive mitochondrial-Y chromosome epistasis.

2020-07-30 | GSE155395 | GEO

Mitochondrial - Y Chromosome Epistasis in Drosophila melanogaster

Project description:Mitochondrial - Y Chromosome Epistasis in Drosophila melanogaster

| PRJNA649569 | ENA

Divergent evolutionary strategies for selective sex chromosome regulation in Drosophila

Project description:The dosage compensation complex (DCC) of Drosophila identifies its X chromosomal binding sites with exquisite selectivity. The principles that assure this vital targeting are known from the D. melanogaster model: DCC-intrinsic specificity of DNA binding, cooperativity with the CLAMP protein, and non-coding roX2 RNA transcribed from the X chromosome. We found that in D. virilis, a species separated from melanogaster by 40 million years of evolution, all principles are active, but contribute differently to X-specificity. In melanogaster, the DCC subunit MSL2 evolved intrinsic DNA-binding selectivity for rare PionX sites, which mark the X chromosome. In virilis, PionX sites are abundant and not X-enriched. Accordingly, MSL2 lacks specific recognition. Here, roX2 RNA plays a more instructive role, counteracting a non-productive interaction of CLAMP and modulating DCC binding selectivity. Remarkably, roX2 triggers a low-diffusion chromatin binding mode characteristic of DCC. Evidently, X-specific regulation is achieved by divergent evolution of similar components.

2021-06-23 | PXD023747 | Pride

Pioneer and nonpioneer factor cooperation drives lineage specific chromatin opening [scRNA-seq]

Project description:Pioneer and nonpioneer factor cooperation drives lineage specific chromatin opening [scRNA-seq]

| PRJNA517137 | ENA