Caenorhabditis elegans
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ABSTRACT:
PROVIDER: PRJNA316338 | ENA |
REPOSITORIES: ENA
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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
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 | GSE128564 | GEO
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
Project description:The execution of developmental programs of gene expression requires an accurate partitioning of the genome into distinct compartments, with heterochromatin enriched at the nuclear periphery. In C. elegans embryonic cells, the methylation of histone H3 lysine 9 (H3K9me) is critical for peripheral anchoring via the chromodomain protein CEC-4, while alternative, H3K9me-independent pathway(s) function in differentiated tissues. An RNAi screen unexpectedly identified the euchromatin factor MRG-1, which binds H3K36me2/me3 domains, as necessary for heterochromatin sequestration in differentiated cells. The data in this submission refer to the identification of chromatin enriched at the nuclear periphery (as measured by interaction with Dam::EMR-1) in intestinal cells of control, singly depleted cec-4 or mrg-1 or doubly depleted cec-4 mrg-1 animals.
2019-04-12 | GSE126028 | GEO
Project description:Higher order chromosome structure and nuclear architecture can have profound effects on gene regulation. We analyzed how compartmentalizing the genome by tethering heterochromatic regions to the nuclear lamina affects dosage compensation in the nematode C. elegans. In this organism, the dosage compensation complex (DCC) binds both X chromosomes of hermaphrodites to repress transcription two-fold, thus balancing gene expression between XX hermaphrodites and XO males. X chromosome structure is disrupted by mutations in DCC subunits. Using X chromosome paint fluorescence microscopy, we found that X chromosome structure and subnuclear localization are also disrupted when the mechanisms that anchor heterochromatin to the nuclear lamina are defective. Strikingly, the heterochromatic left end of the X chromosome is less affected than the gene-rich middle region, which lacks heterochromatic anchors. These changes in X chromosome structure and subnuclear localization are accompanied by small, but significant levels of derepression of X-linked genes as measured by RNA-seq, without any observable defects in DCC localization and DCC-mediated changes in histone modifications. We propose a model in which heterochromatic tethers on the left arm of the X cooperate with the DCC to compact and peripherally relocate the X chromosomes, contributing to gene repression.
2016-03-25 | GSE79597 | GEO
Project description:Binding of the C. elegans dosage compensation complex protein DPY-27
| PRJNA184364 | ENA
Project description:Condensin-Driven Remodeling of X-Chromosome Topology during Dosage Compensation [Hi-C]
| PRJNA268850 | ENA
Project description:Condensin-Driven Remodeling of X-Chromosome Topology during Dosage Compensation [ChIP-Seq]
| PRJNA255675 | ENA
Project description:Condensin-Driven Remodeling of X-Chromosome Topology during Dosage Compensation [RNA-Seq]
| PRJNA256014 | ENA
Project description:H4K20me1 contributes to downregulation of X-linked genes for Caenorhabditis elegans dosage compensation
| PRJNA171711 | ENA