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Transcription dosage compensation does not occur in Down syndrome

ABSTRACT: Transcription dosage compensation does not occur in Down syndrome

PROVIDER: PRJNA962941 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24348200.fastq.gz	Fastqsanger.gz
	SRR24348201.fastq.gz	Fastqsanger.gz
	SRR24348202.fastq.gz	Fastqsanger.gz
	SRR24348203.fastq.gz	Fastqsanger.gz
	SRR24348204.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription dosage compensation does not occur in Down syndrome.

Project description:BackgroundThe increase in DNA copy number in Down syndrome (DS; caused by trisomy 21) has led to the DNA dosage hypothesis, which posits that the level of gene expression is proportional to the gene's DNA copy number. Yet many reports have suggested that a proportion of chromosome 21 genes are dosage compensated back towards typical expression levels (1.0×). In contrast, other reports suggest that dosage compensation is not a common mechanism of gene regulation in trisomy 21, providing support to the DNA dosage hypothesis.ResultsIn our work, we use both simulated and real data to dissect the elements of differential expression analysis that can lead to the appearance of dosage compensation, even when compensation is demonstrably absent. Using lymphoblastoid cell lines derived from a family with an individual with Down syndrome, we demonstrate that dosage compensation is nearly absent at both nascent transcription (GRO-seq) and steady-state RNA (RNA-seq) levels. Furthermore, we link the limited apparent dosage compensation to expected allelic variation in transcription levels.ConclusionsTranscription dosage compensation does not occur in Down syndrome. Simulated data containing no dosage compensation can appear to have dosage compensation when analyzed via standard methods. Moreover, some chromosome 21 genes that appear to be dosage compensated are consistent with allele specific expression.

| S-EPMC10636926 | biostudies-literature

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

Project description:Transcription dosage compensation does not occur in Down syndrome

| PRJNA966937 | ENA

Transcription dosage compensation does not occur in Down syndrome

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

2023-04-28 | GSE230999 | GEO

Binding of the C. elegans dosage compensation complex protein DPY-27

Project description:Dosage Compensation is required to correct for uneven gene dose between the sexes. We utilized global run-on sequencing (GRO-seq) to examine how Caenorhabditis elegans dosage compensation reduces transcription of X-linked genes. To facilitate these experiments, we required accurate 5’-ends of genes that have been missing due to a co-transcriptional trans-splicing event common in nematodes. We developed a modified GRO-seq protocol to identify TSSs that are supported by transcription, and determined that TSSs lie more than 1 kb upstream of the previously annotated TSS for nearly one-quarter of all genes. We then investigated the changes that occur in transcriptionally engaged RNA Polymerase when dosage compensation is disrupted, and find that dosage compensation controls recruitment of RNA Polymerase to X-linked genes.

2013-06-18 | GSE43086 | GEO

Binding of the C. elegans dosage compensation complex protein DPY-27

Project description:Dosage Compensation is required to correct for uneven gene dose between the sexes. We utilized global run-on sequencing (GRO-seq) to examine how Caenorhabditis elegans dosage compensation reduces transcription of X-linked genes. To facilitate these experiments, we required accurate 5M-bM-^@M-^Y-ends of genes that have been missing due to a co-transcriptional trans-splicing event common in nematodes. We developed a modified GRO-seq protocol to identify TSSs that are supported by transcription, and determined that TSSs lie more than 1 kb upstream of the previously annotated TSS for nearly one-quarter of all genes. We then investigated the changes that occur in transcriptionally engaged RNA Polymerase when dosage compensation is disrupted, and find that dosage compensation controls recruitment of RNA Polymerase to X-linked genes. Two biological replicates of ChIP with DPY-27 and a random rabbit IgG

2013-06-18 | E-GEOD-43086 | biostudies-arrayexpress

Down Syndrome

Project description:Down Syndrome

| PRJNA804910 | ENA

Trisomy 21 Dosage Compensation Map (T21DoCoMap)

Project description:Trisomy 21 Dosage Compensation Map (T21DoCoMap)

| PRJNA720724 | ENA

Trisomy 21 Dosage Compensation Map (T21DoCoMap)

Project description:Trisomy 21 Dosage Compensation Map (T21DoCoMap)

| PRJNA720725 | ENA

RNA stability controlled by m6A methylation contributes to X-to-autosome dosage compensation in mammals

Project description:In mammals, X-chromosomal genes are expressed from a single copy since males (XY) possess a single X chromosome, while females (XX) undergo X inactivation. To compensate for this reduction in dosage compared to two active copies of autosomes, it has been proposed that genes from the active X chromosome exhibit dosage compensation. However, the existence and mechanism of X-to-autosome dosage compensation are still under debate. Here, we show that X-chromosomal transcripts are reduced in m6A modifications and more stable compared to their autosomal counterparts. Acute depletion of m6A selectively stabilises autosomal transcripts, resulting in perturbed dosage compensation in mouse embryonic stem cells. We propose that higher stability of X-chromosomal transcripts is directed by lower levels of m6A, indicating that mammalian dosage compensation is partly regulated by epitranscriptomic RNA modifications.

| EGAS00001007112 | EGA

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