Condensin I folds the C. elegans genome [RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA821226 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Condensin I folds the C. elegans genome
| PRJNA821234 | ENA
Project description:Condensin I folds the C. elegans genome [Hi-C]
| PRJNA821239 | ENA
Project description:Condensin I folds the C. elegans genome [Ribo-Zero-seq]
| PRJNA821236 | ENA
Project description:Structural Maintenance of chromosomes (SMC) complexes, cohesin and condensins, have been named after their roles during meiosis and mitosis. Recent data in mammalian cells and Drosophila have described the additional role of cohesin for genome folding into loops and domains during interphase. However, determinants of genome folding in holocentric species remain unclear. Using high resolution chromosome conformation capture, we show that overlapping large-scale nuclear localization and small-scale epigenomic states compartmentalize the C. elegans genome. By systematically and acutely inactivating each SMC complex, we observe that in contrast to other studied systems, cohesin creates small loops, while condensin I has a major role in genome folding: its inactivation causes genome-wide decompaction, chromosome mixing, loss of loops and TAD structures and reinforcement of fine-scale epigenomic compartments. Counter-intuitively, removal of condensin I and its X-specific variant condensin IDC from the X chromosomes led to the formation of a loop compartment coinciding with a subset of previously characterized loading sites for condensin IDC and bound by the X-targeting complex SDC. While transcriptional changes were limited for all autosomes upon cohesin and condensin II inactivation, removal of condensin I/IDC from the X chromosome led to transcriptional up-regulation of X-linked genes demonstrating that a sustained role for condensin IDC in gene regulation. Finally, while condensin I inactivation leads to reduced lifespan, we show that this reduction is due to X-specific gene upregulation rather than global genome decompaction.
2024-04-18 | GSE199717 | GEO
Project description:Structural Maintenance of chromosomes (SMC) complexes, cohesin and condensins, have been named after their roles during meiosis and mitosis. Recent data in mammalian cells and Drosophila have described the additional role of cohesin for genome folding into loops and domains during interphase. However, determinants of genome folding in holocentric species remain unclear. Using high resolution chromosome conformation capture, we show that overlapping large-scale nuclear localization and small-scale epigenomic states compartmentalize the C. elegans genome. By systematically and acutely inactivating each SMC complex, we observe that in contrast to other studied systems, cohesin creates small loops, while condensin I has a major role in genome folding: its inactivation causes genome-wide decompaction, chromosome mixing, loss of loops and TAD structures and reinforcement of fine-scale epigenomic compartments. Counter-intuitively, removal of condensin I and its X-specific variant condensin IDC from the X chromosomes led to the formation of a loop compartment coinciding with a subset of previously characterized loading sites for condensin IDC and bound by the X-targeting complex SDC. While transcriptional changes were limited for all autosomes upon cohesin and condensin II inactivation, removal of condensin I/IDC from the X chromosome led to transcriptional up-regulation of X-linked genes demonstrating that a sustained role for condensin IDC in gene regulation. Finally, while condensin I inactivation leads to reduced lifespan, we show that this reduction is due to X-specific gene upregulation rather than global genome decompaction.
2024-04-18 | GSE199719 | GEO
Project description:Structural Maintenance of chromosomes (SMC) complexes, cohesin and condensins, have been named after their roles during meiosis and mitosis. Recent data in mammalian cells and Drosophila have described the additional role of cohesin for genome folding into loops and domains during interphase. However, determinants of genome folding in holocentric species remain unclear. Using high resolution chromosome conformation capture, we show that overlapping large-scale nuclear localization and small-scale epigenomic states compartmentalize the C. elegans genome. By systematically and acutely inactivating each SMC complex, we observe that in contrast to other studied systems, cohesin creates small loops, while condensin I has a major role in genome folding: its inactivation causes genome-wide decompaction, chromosome mixing, loss of loops and TAD structures and reinforcement of fine-scale epigenomic compartments. Counter-intuitively, removal of condensin I and its X-specific variant condensin IDC from the X chromosomes led to the formation of a loop compartment coinciding with a subset of previously characterized loading sites for condensin IDC and bound by the X-targeting complex SDC. While transcriptional changes were limited for all autosomes upon cohesin and condensin II inactivation, removal of condensin I/IDC from the X chromosome led to transcriptional up-regulation of X-linked genes demonstrating that a sustained role for condensin IDC in gene regulation. Finally, while condensin I inactivation leads to reduced lifespan, we show that this reduction is due to X-specific gene upregulation rather than global genome decompaction.
2024-04-18 | GSE199721 | GEO
Project description:Condensins are multi-subunit protein complexes that regulate chromosome structure throughout cell-cycle. Metazoans contain two types of condensin complexes (I and II) with essential and distinct functions. In C. elegans a third type of condensin (IDC) functions as part of the X chromosome dosage compensation complex1,2. We mapped genome-wide binding sites of the three condensin types in C. elegans embryos. Characteristics of condensin binding are similar between condensin types. ChIP-seq profiles of C. elegans subunits of the three condensins in 3-6 replicates from mixed stage embryos, controls are included, and RNA-Seq profiles of C. elegans in 5 replicates from mixed staged embryos. Additionally, ChIP-seq profiles of the condensin II subunit KLE-2 in 6 replicates from L3 with controls, and RNA-Seq profiles of KLE-2 mutants in 3 replicates each from L3.
2013-09-16 | E-GEOD-45678 | biostudies-arrayexpress
Project description:Condensins are multi-subunit protein complexes that regulate chromosome structure throughout cell-cycle. Metazoans contain two types of condensin complexes (I and II) with essential and distinct functions. In C. elegans a third type of condensin (IDC) functions as part of the X chromosome dosage compensation complex1,2. We mapped genome-wide binding sites of the three condensin types in C. elegans embryos. Characteristics of condensin binding are similar between condensin types.
2013-09-16 | GSE45678 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-04-17 | GSE199723 | GEO
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 | GSE168802 | GEO