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X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation [ChIP-seq]

ABSTRACT: X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation [ChIP-seq]

PROVIDER: PRJNA528109 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8754480.fastq.gz	Fastqsanger.gz
	SRR8754490.fastq.gz	Fastqsanger.gz
	SRR8754481.fastq.gz	Fastqsanger.gz
	SRR8754491.fastq.gz	Fastqsanger.gz
	SRR8754482.fastq.gz	Fastqsanger.gz

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X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation

Project description:X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation

| PRJNA528108 | ENA

X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation [RNA-seq]

Project description:Mechanisms establishing higher-order chromosome structures and their roles in gene regulation are elusive. We analyzed chromosome architecture during nematode X-chromosome dosage compensation, which represses transcription via a dosage-compensation condensin complex (DCC) that binds hermaphrodite Xs and establishes megabase-size topologically associating domains (TADs). We show that DCC binding at high-occupancy sites (rex sites) defines eight TAD boundary locations. Single rex deletions disrupted boundaries, and single insertions created new boundaries, demonstrating one rex site is necessary and sufficient for DCC-dependent boundary formation. Deleting eight rex sites (8rexΔ) recapitulated TAD structure of DCC mutants, permitting analysis when chromosome-wide domain architecture was disrupted but most DCC binding remained. 8rexΔ animals exhibited no changes in X expression and lacked dosage-compensation mutant phenotypes. Hence, TAD boundaries are neither the cause nor consequence of gene repression during dosage compensation. Abrogating TAD structure did, however, reduce thermotolerance, accelerate aging, and shorten lifespan, implicating chromosome architecture in regulating stress responses and aging.

2019-09-05 | GSE128566 | GEO

X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation [ChIP-seq]

2019-09-05 | GSE128564 | GEO

X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation [Hi-C]

2019-09-05 | GSE128559 | GEO

X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation [Hi-C]

Project description:X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation [Hi-C]

| PRJNA528104 | ENA

X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation [RNA-seq]

Project description:X chromosome domain architecture regulates Caenorhabditis elegans lifespan but not dosage compensation [RNA-seq]

| PRJNA528111 | ENA

X Chromosome Domain Architecture Regulates Caenorhabditis elegans Lifespan but Not Dosage Compensation.

Project description:Mechanisms establishing higher-order chromosome structures and their roles in gene regulation are elusive. We analyzed chromosome architecture during nematode X chromosome dosage compensation, which represses transcription via a dosage-compensation condensin complex (DCC) that binds hermaphrodite Xs and establishes megabase-sized topologically associating domains (TADs). We show that DCC binding at high-occupancy sites (rex sites) defines eight TAD boundaries. Single rex deletions disrupted boundaries, and single insertions created new boundaries, demonstrating that a rex site is necessary and sufficient to define DCC-dependent boundary locations. Deleting eight rex sites (8rexΔ) recapitulated TAD structure of DCC mutants, permitting analysis when chromosome-wide domain architecture was disrupted but most DCC binding remained. 8rexΔ animals exhibited no changes in X expression and lacked dosage-compensation mutant phenotypes. Hence, TAD boundaries are neither the cause nor the consequence of DCC-mediated gene repression. Abrogating TAD structure did, however, reduce thermotolerance, accelerate aging, and shorten lifespan, implicating chromosome architecture in stress responses and aging.

| S-EPMC6810858 | biostudies-literature

X-chromosome dosage compensation dynamics in human early embryos

Project description:Studying X-chromosome dosage compensation dynamics in human early embryos using single cell RNA sequencing

2019-10-24 | GSE130050 | 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

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

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