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

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

PROVIDER: PRJNA528104 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8754260_1.fastq.gz	Fastqsanger.gz
	SRR8754260_2.fastq.gz	Fastqsanger.gz
	SRR8754270_1.fastq.gz	Fastqsanger.gz
	SRR8754270_2.fastq.gz	Fastqsanger.gz
	SRR8754261_1.fastq.gz	Fastqsanger.gz

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

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 | GSE128559 | 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 [RNA-seq]

2019-09-05 | GSE128566 | GEO

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 [ChIP-seq]

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

| PRJNA528109 | 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

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

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

SMC-mediated dosage compensation in C. elegans evolved in the presence of an ancestral nematode mechanism [Hi-C]

Project description:Mechanisms of X chromosome dosage compensation have been studied extensively in a few model species representing clades of shared sex chromosome ancestry. However, the diversity within each clade as a function of sex chromosome evolution is largely unknown. Here, we anchor ourselves to the nematode Caenorhabditis elegans, for which a well-studied mechanism of dosage compensation occurs through a specialized structural maintenance of chromosomes (SMC) complex, and explore the diversity of dosage compensation in the surrounding phylogeny of nematodes. Through phylogenetic analysis of the C. elegans dosage compensation complex and a survey of its epigenetic signatures, including X-specific topologically associating domains (TADs) and X-enrichment of H4K20me1, we found that the condensin-mediated mechanism evolved recently in the lineage leading to Caenorhabditis through an SMC-4 duplication. Intriguingly, an independent duplication of SMC-4 and the presence of X-specific TADs in Pristionchus pacificus suggest that condensin-mediated dosage compensation arose more than once. mRNA-seq analyses of gene expression in several nematode species indicate that dosage compensation itself is ancestral, as expected from the ancient XO sex determination system. Indicative of the ancestral mechanism, H4K20me1 is enriched on the X chromosomes in Oscheius tipulae, which does not contain X-specific TADs or SMC-4 paralogs. Together, our results indicate that the dosage compensation system in C. elegans is surprisingly new, and condensin may have been co-opted repeatedly in nematodes, suggesting that the process of evolving a chromosome-wide gene regulatory mechanism for dosage compensation is constrained.

2024-05-21 | GSE267963 | GEO

SDC-3 subunit of the dosage compensation complex in wild-type N2 C. elegans and Hi-C in C' elegans strains with deleted rex and extra rex sites

Project description:ChIP-seq for the SDC-3 subunit of the dosage compensation complex in wild-type N2 C. elegans and Hi-C in C' elegans strains with deleted rex and extra rex sites

2022-09-01 | GSE205949 | GEO

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