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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [ChIP-seq]

ABSTRACT: Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [ChIP-seq]

PROVIDER: PRJNA524292 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8632340.fastq.gz	Fastqsanger.gz
	SRR8632350_1.fastq.gz	Fastqsanger.gz
	SRR8632350_2.fastq.gz	Fastqsanger.gz
	SRR8632341.fastq.gz	Fastqsanger.gz
	SRR8632351_1.fastq.gz	Fastqsanger.gz

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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome

Project description:Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome

| PRJNA524287 | ENA

Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [RNA-seq]

Project description:Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [RNA-seq]

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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [RNA-seq]

Project description:In D. melanogaster males, X chromosome monosomy is compensated by chromosome-wide transcription activation. We found that complete dosage compensation during embryogenesis takes surprisingly long. Although the activating Dosage Compensation Complex (DCC) associates with the chromosome and acetylates histone H4 early, many genes are not compensated. Acetylation levels on gene bodies continue to increase for several hours after gastrulation in parallel with progressive compensation. Constitutive genes are compensated earlier than developmental genes. Remarkably, later compensation correlates with longer distances to DCC binding sites. This time-space relationship suggests that DCC action on target genes requires maturation of the active chromosome compartment.

2019-06-28 | GSE127176 | GEO

Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [ChIP-seq]

2019-06-28 | GSE127175 | GEO

Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement.

Project description:In Drosophila melanogaster males, X-chromosome monosomy is compensated by chromosome-wide transcription activation. We found that complete dosage compensation during embryogenesis takes surprisingly long and is incomplete even after 10 h of development. Although the activating dosage compensation complex (DCC) associates with the X-chromosome and MOF acetylates histone H4 early, many genes are not compensated. Acetylation levels on gene bodies continue to increase for several hours after gastrulation in parallel with progressive compensation. Constitutive genes are compensated earlier than developmental genes. Remarkably, later compensation correlates with longer distances to DCC binding sites. This time-space relationship suggests that DCC action on target genes requires maturation of the active chromosome compartment.

| S-EPMC6680166 | biostudies-literature

Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-06-28 | GSE127177 | GEO

Dosage compensation mass spectrometry in platypus, chicken and mouse

Project description:Gene dosage imbalance of heteromorphic sex chromosomes (XY or ZW) exists between the sexes, and with the autosomes. Mammalian X chromosome inactivation was long thought to imply a critical need for dosage compensation in vertebrates. However, mRNA abundance measurements that demonstrated sex chromosome transcripts are neither balanced between the sexes or with autosomes in monotreme mammals or birds brought sex chromosome dosage compensation into question. This study examines transcriptomic and proteomic levels of dosage compensation in platypus and chicken compared to mouse, a model eutherian species. We analyzed mRNA and protein levels in heart and liver tissues of chicken, mouse and platypus.

2024-07-30 | PXD040182 | Pride

Dosage Compensation of an Aneuploid Genome in Mouse Spermatogenic Cells

Project description:Autosomal trisomies and monosomies bring serious threats to embryonic development through transcriptional disarray primarily caused by the dosage effect of the aneuploid part of the genome. The present study compared the effect of a mouse viable 30 Mb segmental trisomy on the genome-wide transcriptional profile of somatic (liver) cells and male germ cells. While the 1.6-fold change in expression of triplicated genes reflected the gene dosage in liver cells, the extra copy was almost fully compensated in early pachytene spermatocytes, showing 1.18-fold increase. Allele-specific semi-quantitative evaluation of steady-state mRNA levels of the triplicated Amdhd2 gene revealed silencing evenly distributed among all three copies in these meiotic cells. Although more pronounced, the dosage compensation of trisomic genes was concordant with the incidence of HORMAD2 and γH2AX markers of unsynapsed chromatin. The possible explanations include insufficient sensitivity to detect both MSUC markers in the 30 Mb region of the chromosome, or an early silencing effect of another epigenetic factor. Taken together, our results indicate that the meiotic silencing of unsynapsed chromatin is the major but not the only factor driving the dosage compensation of triplicated genes in primary spermatocytes.

2016-03-30 | GSE54683 | GEO

Dosage Compensation of an Aneuploid Genome in Mouse Spermatogenic Cells

Project description:Autosomal trisomies and monosomies bring serious threats to embryonic development through transcriptional disarray primarily caused by the dosage effect of the aneuploid part of the genome. The present study compared the effect of a mouse viable 30 Mb segmental trisomy on the genome-wide transcriptional profile of somatic (liver) cells and male germ cells. While the 1.6-fold change in expression of triplicated genes reflected the gene dosage in liver cells, the extra copy was almost fully compensated in early pachytene spermatocytes, showing 1.18-fold increase. Allele-specific semi-quantitative evaluation of steady-state mRNA levels of the triplicated Amdhd2 gene revealed silencing evenly distributed among all three copies in these meiotic cells. Although more pronounced, the dosage compensation of trisomic genes was concordant with the incidence of HORMAD2 and Î³H2AX markers of unsynapsed chromatin. The possible explanations include insufficient sensitivity to detect both MSUC markers in the 30 Mb region of the chromosome, or an early silencing effect of another epigenetic factor. Taken together, our results indicate that the meiotic silencing of unsynapsed chromatin is the major but not the only factor driving the dosage compensation of triplicated genes in primary spermatocytes. We compared the global expression profiles in isolated popoulations of meiotic cells and liver cells of Ts43H trisomic males and their t121/D17 euploid siblings.

2016-03-30 | E-GEOD-54683 | biostudies-arrayexpress

Trisomy 21 Dosage Compensation Map (T21DoCoMap)

Project description:Trisomy 21 Dosage Compensation Map (T21DoCoMap)

| PRJNA720724 | ENA