Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA114437 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:DCC binding and function (ChIP-chip: DPY-27)
| PRJNA114415 | ENA
Project description:DCC binding and function (ChIP-chip: SDC-2)
| PRJNA114417 | ENA
Project description:DCC binding and function (ChIP-chip: SDC-3, DPY-27, Mock)
| PRJNA114419 | ENA
Project description:DCC binding and function (ChIP-chip: SDC-3, MIX-1, DPY-27, Mock)
| PRJNA114439 | ENA
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:Examination of DPY-30, DPY-27, SDC-3, DPY-26, MIX-1, SMC-4, ASH-2, RNA Polymerase II binding in wild type and DCC mutant embryos
| PRJNA142503 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE14649: DCC binding and function (Expression Analysis) GSE14650: DCC binding and function (ChIP-chip: SDC-3, MIX-1, DPY-27, Mock) GSE14651: DCC binding and function (ChIP-chip: DPY-27) GSE14652: DCC binding and function (ChIP-chip: SDC-2) GSE14653: DCC binding and function (ChIP-chip: SDC-3, DPY-27, Mock) Refer to individual Series
2010-05-22 | E-GEOD-14640 | biostudies-arrayexpress
Project description:RNA sequencing analysis of DAF-16 target gene expression when math-33 function is genetically inactivated
| PRJNA287674 | ENA