A Mediator-cohesin axis controls heterochromatin domain formation [ChIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA516928 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12096590.fastq.gz | Fastqsanger.gz | |||
| SRR12096591.fastq.gz | Fastqsanger.gz | |||
| SRR12096592.fastq.gz | Fastqsanger.gz | |||
| SRR12096593.fastq.gz | Fastqsanger.gz | |||
| SRR12096594.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:A Mediator-cohesin axis controls heterochromatin domain formation
| PRJNA516941 | ENA
Project description:A Mediator-cohesin axis controls heterochromatin domain formation.
| PRJNA517136 | ENA
Project description:The genome consists of regions of transcriptionally active euchromatin and more silent heterochromatin. We reveal that the formation of heterochromatin domains requires cohesin turnover on DNA. Stabilization of cohesin on DNA through depletion of its release factor WAPL leads to a near-complete loss of heterochromatin domains. The Mediator CDK module controls heterochromatin in an opposing manner. Loss of this module leads to an almost binary partition of the genome into dense H3K9me3 domains, and regions devoid of H3K9me3 spanning the rest of the genome. By restricting the degree of heterochromatinization, the Mediator CDK module creates a transcription-permissive context that enables gene expression within heterochromatin domains. WAPL deficiency prevents the formation of heterochromatin domains, thus allowing for gene expression even in the absence of the Mediator CDK module. We propose that heterochromatin is controlled by two opposing activities, in which the Mediator CDK module and cohesin turnover must be balanced to enable the correct distribution of epigenetic marks to ensure proper gene expression.
2022-01-11 | GSE125631 | GEO
Project description:The genome consists of regions of transcriptionally active euchromatin and more silent heterochromatin. We reveal that the formation of heterochromatin domains requires cohesin turnover on DNA. Stabilization of cohesin on DNA through depletion of its release factor WAPL leads to a near-complete loss of heterochromatin domains. The Mediator CDK module controls heterochromatin in an opposing manner. Loss of this module leads to an almost binary partition of the genome into dense H3K9me3 domains, and regions devoid of H3K9me3 spanning the rest of the genome. By restricting the degree of heterochromatinization, the Mediator CDK module creates a transcription-permissive context that enables gene expression within heterochromatin domains. WAPL deficiency prevents the formation of heterochromatin domains, thus allowing for gene expression even in the absence of the Mediator CDK module. We propose that heterochromatin is controlled by two opposing activities, in which the Mediator CDK module and cohesin turnover must be balanced to enable the correct distribution of epigenetic marks to ensure proper gene expression.
2022-01-11 | GSE125618 | GEO
Project description:The genome consists of regions of transcriptionally active euchromatin and more silent heterochromatin. We reveal that the formation of heterochromatin domains requires cohesin turnover on DNA. Stabilization of cohesin on DNA through depletion of its release factor WAPL leads to a near-complete loss of heterochromatin domains. The Mediator CDK module controls heterochromatin in an opposing manner. Loss of this module leads to an almost binary partition of the genome into dense H3K9me3 domains, and regions devoid of H3K9me3 spanning the rest of the genome. By restricting the degree of heterochromatinization, the Mediator CDK module creates a transcription-permissive context that enables gene expression within heterochromatin domains. WAPL deficiency prevents the formation of heterochromatin domains, thus allowing for gene expression even in the absence of the Mediator CDK module. We propose that heterochromatin is controlled by two opposing activities, in which the Mediator CDK module and cohesin turnover must be balanced to enable the correct distribution of epigenetic marks to ensure proper gene expression.
2022-01-11 | GSE125622 | GEO
Project description:A Mediator-cohesin axis controls heterochromatin domain formation [RNA-seq]
| PRJNA516925 | ENA
Project description:The genome consists of regions of transcriptionally active euchromatin and more silent heterochromatin. We reveal that the formation of heterochromatin domains requires cohesin turnover on DNA. Stabilization of cohesin on DNA through depletion of its release factor WAPL leads to a near-complete loss of heterochromatin domains. We observe the opposite phenotype in cells deficient for subunits of the Mediator-CDK module, with an almost binary partition of the genome into dense H3K9me3 domains, and regions devoid of H3K9me3 spanning the rest of the genome. We suggest that the Mediator-CDK module might contribute to gene expression by limiting the formation of dense heterochromatin domains. WAPL deficiency prevents the formation of heterochromatin domains, and allows for gene expression even in the absence of the Mediator-CDK subunit MED12. We propose that cohesin and Mediator affect heterochromatin in different ways to enable the correct distribution of epigenetic marks, and thus to ensure proper gene expression.
| S-EPMC8826356 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-01-11 | GSE125672 | GEO
Project description:Background: Heterochromatin at the pericentromeric repeats in fission yeast is assembled and spread by an RNAi-dependent mechanism, which is coupled to the transcription of non-coding RNA from the repeats by RNA polymerase II. In addition, Rrp6, a component of the nuclear exosome, also contributes to heterochromatin assembly and is coupled to non-coding RNA transcription. The multi-subunit complex Mediator, which directs initiation of RNA polymerase II-dependent transcription, has recently been suggested to function after initiation in processes such as elongation of transcription and splicing. However, the role of Mediator in the regulation of chromatin structure is not well understood. Results: We investigated the role of Mediator in pericentromeric heterochromatin formation and found that deletion of specific subunits of the head domain of Mediator compromised heterochromatin structure. The Mediator head domain was required for Rrp6-dependent heterochromatin nucleation at the pericentromere and for RNAi-dependent spreading of heterochromatin into the neighboring region. In the latter process, Mediator appeared to contribute to efficient processing of siRNA from transcribed non-coding RNA, which was required for efficient spreading of heterochromatin. Furthermore, the head domain directed efficient transcription in heterochromatin. Conclusions: These results reveal a pivotal role for Mediator in multiple steps of transcription-coupled formation of pericentromeric heterochromatin. This observation further extends the role of Mediator to co-transcriptional chromatin regulation. Gene expression profile at exponentially-growing phase.in the fission yeast deletion mutants of pmc6, med20 and dcr1.
2013-08-31 | E-GEOD-43543 | biostudies-arrayexpress
Project description:Background: Heterochromatin at the pericentromeric repeats in fission yeast is assembled and spread by an RNAi-dependent mechanism, which is coupled to the transcription of non-coding RNA from the repeats by RNA polymerase II. In addition, Rrp6, a component of the nuclear exosome, also contributes to heterochromatin assembly and is coupled to non-coding RNA transcription. The multi-subunit complex Mediator, which directs initiation of RNA polymerase II-dependent transcription, has recently been suggested to function after initiation in processes such as elongation of transcription and splicing. However, the role of Mediator in the regulation of chromatin structure is not well understood. Results: We investigated the role of Mediator in pericentromeric heterochromatin formation and found that deletion of specific subunits of the head domain of Mediator compromised heterochromatin structure. The Mediator head domain was required for Rrp6-dependent heterochromatin nucleation at the pericentromere and for RNAi-dependent spreading of heterochromatin into the neighboring region. In the latter process, Mediator appeared to contribute to efficient processing of siRNA from transcribed non-coding RNA, which was required for efficient spreading of heterochromatin. Furthermore, the head domain directed efficient transcription in heterochromatin. Conclusions: These results reveal a pivotal role for Mediator in multiple steps of transcription-coupled formation of pericentromeric heterochromatin. This observation further extends the role of Mediator to co-transcriptional chromatin regulation.
2013-08-31 | GSE43543 | GEO