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Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans (ChIP-seq and Hi-C data)

ABSTRACT: Inspection of Hi-C and ChIP-seq data suggests that condensin DC is an X-chromosome enriched loop extruder that stalls at rex sites. Insertion of rex site on X-chromosome suggests orientation independent barrier function of rex sites. Insertion of rex site on chromosome-II results in recruitment and spreading of condensin DC that coincides with TAD formation.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE206065 | GEO | 2022/06/14

REPOSITORIES: GEO

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Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans (ChIP-seq)

Project description:Condensins are molecular motors that compact DNA for chromosome segregation and gene regulation. In vitro experiments have begun to elucidate the mechanics of condensin function but how condensin loading and translocation along DNA controls eukaryotic chromosome structure in vivo remains poorly understood. To address this question, we took advantage of a specialized condensin, which organizes the 3D conformation of X chromosomes to mediate dosage compensation (DC) in C. elegans. Condensin DC is recruited and spreads from a small number of recruitment elements on the X chromosome (rex). We found that ectopic insertion of rex sites on an autosome leads to bidirectional spreading of the complex over hundreds of kilobases. On the X chromosome, strong rex sites contain multiple copies of a 12-bp sequence motif and act as TAD borders. Inserting a strong rex and ectopically recruiting the complex on the X chromosome or an autosome creates a loop-anchored TAD. Unlike the CTCF system, which controls TAD formation by cohesin, direction of the 12-bp motif does not control the specificity of loops. In an X;V fusion chromosome, condensin DC linearly spreads into V and increases 3D DNA contacts, but fails to form TADs in the absence of rex sites. Finally, we provide in vivo evidence for the loop extrusion hypothesis by targeting multiple dCas9-Suntag complexes to an X chromosome repeat region. Consistent with linear translocation along DNA, condensin DC accumulates at the block site. Together, our results support a model whereby strong rex sites act as insulation elements through recruitment and bidirectional spreading of condensin DC molecules and form loop-anchored TADs.

2021-03-24 | GSE169250 | GEO

Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans (RNA-seq)

2021-03-24 | GSE168802 | GEO

Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans (Hi-C)

2021-03-24 | GSE169468 | GEO

Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans

Project description:Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans

| PRJNA714064 | ENA

Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans

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

2021-03-23 | GSE168803 | GEO

Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans (ChIP-seq)

Project description:Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans (ChIP-seq)

| PRJNA716063 | ENA

Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans (RNA-seq)

Project description:Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans (RNA-seq)

| PRJNA714067 | ENA

Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans (Hi-C)

Project description:Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans (Hi-C)

| PRJNA716654 | 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

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