CTCF blocks anti-sense transcription initiation at divergent gene promoters
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA725532 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14336877_1.fastq.gz | Fastqsanger.gz | |||
| SRR14336877_2.fastq.gz | Fastqsanger.gz | |||
| SRR14336878_1.fastq.gz | Fastqsanger.gz | |||
| SRR14336878_2.fastq.gz | Fastqsanger.gz | |||
| SRR14336879_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Transcription is typically divergent, initiating at closely spaced oppositely oriented core promoters to produce sense and unstable upstream antisense transcripts (uasTrx). How antisense transcription is regulated and coordinated with sense transcription is largely unknown. Here by combining acute degradation of the multi-functional transcription factor CTCF and nascent transcription measurements, we find that CTCF specifically suppresses antisense but not sense transcription at hundreds of divergent promoters, the great majority of which bear proximal CTCF binding sites. Genome editing, chromatin conformation studies and 5’ transcript mapping revealed that CTCF directly suppresses uasTrx initiation in manner independent of its chromatin architectural function. Primary transcript RNA FISH revealed co-bursting of sense and anti-sense transcripts is disfavored, suggesting CTCF-regulated competition for transcription initiation. In sum, CTCF shapes the noncoding transcriptional landscape by suppressing upstream antisense transcription.
2022-05-02 | GSE173443 | GEO
Project description:Transcription is typically divergent, initiating at closely spaced oppositely oriented core promoters to produce sense and unstable upstream antisense transcripts (uasTrx). How antisense transcription is regulated and coordinated with sense transcription is largely unknown. Here by combining acute degradation of the multi-functional transcription factor CTCF and nascent transcription measurements, we find that CTCF specifically suppresses antisense but not sense transcription at hundreds of divergent promoters, the great majority of which bear proximal CTCF binding sites. Genome editing, chromatin conformation studies and 5’ transcript mapping revealed that CTCF directly suppresses uasTrx initiation in manner independent of its chromatin architectural function. Primary transcript RNA FISH revealed co-bursting of sense and anti-sense transcripts is disfavored, suggesting CTCF-regulated competition for transcription initiation. In sum, CTCF shapes the noncoding transcriptional landscape by suppressing upstream antisense transcription.
2022-05-02 | GSE173442 | GEO
Project description:CTCF blocks anti-sense transcription initiation at divergent gene promoters [ChIP-Seq]
| PRJNA725535 | ENA
Project description:CTCF blocks anti-sense transcription initiation at divergent gene promoters [PRO-Seq]
| PRJNA725536 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-05-02 | GSE173444 | GEO
Project description:Anti-sense transcription originating upstream of mammalian protein-coding genes is a well-documented phenomenon, but remarkably little is known about the function or regulation of these anti-sense promoters or the non-coding RNAs they generate. Here we define at nucleotide resolution the divergent transcription start sites (TSSs) near mouse mRNAs. We find that coupled sense and anti-sense TSSs form the boundaries of an evolutionarily conserved and nucleosome-depleted regulatory region with dramatically enriched transcription factor (TF) occupancy. Notably, as the distance between sense and anti-sense TSSs increases, so does the level of TF binding and signal-dependent gene activation. We further discover a cluster of anti-sense TSSs in macrophages with an enhancer-like chromatin signature. Remarkably, this signature identifies promoters that are selectively and rapidly activated during immune challenge. We conclude that anti-sense TSSs can serve as potent, local enhancers of sense-strand gene expression by facilitating TF binding and deposition of activating histone modifications.
2015-06-23 | GSE62151 | GEO
Project description:Mammalian transcriptomes are complex and formed by extensive promoter activity. Moreover, gene promoters are largely divergent and initiate transcription of reverse-oriented promoter upstream transcripts (PROMPTs). Although PROMPTs are commonly terminated early, influenced by early polyadenylation (pA) sites, promoters often cluster so that the divergent activity of one might impact another. Here, we find that the distance between promoters strongly correlates with the expression, stability and length of their associated PROMPTs. Adjacent promoters driving divergent mRNA transcription support PROMPT formation, but due to pA site constraints, these transcripts tend to spread into the neighboring mRNA on the same strand. This mechanism to derive new alternative mRNA transcription start sites (TSSs) is also evident at closely spaced promoters supporting convergent mRNA transcription. We suggest that basic building blocks of divergently transcribed core promoter pairs, in combination with the wealth of TSSs in mammalian genomes, provides a framework with which evolution shapes transcriptomes. Mapping of paired 5â?? and 3â??ends of capped and polyadenylated RNAs from RRP40-depleted and eGFP control HeLa cells and using transcript isoform sequencing (TIF-Seq, see Pelechano et al. Nat Protoc 2014 (PMID: 24967623) and Pelechano et al. Nature 2013 (PMID: 23615609)).
2016-05-13 | E-GEOD-75183 | biostudies-arrayexpress
Project description:The directionality of gene promoters, the proportion of protein coding over divergent noncoding transcription, is highly variable and regulated. How promoter directionality is controlled remains poorly understood. We show that chromatin remodelling complex RSC, general regulatory factors (GRFs) including transcription factors (TFs) can facilitate promoter directionality by attenuating divergent noncoding transcription. Depletion of RSC increased divergent noncoding and decreased protein coding transcription of promoters with strong directionality. Consistent with RSC’s role in regulating chromatin, RSC depletion negatively impacts nucleosome positions upstream of the nucleosome depleted region where divergent transcription initiates, suggesting that nucleosome positioning upstream in promoters physically blocks the recruitment of transcription machinery. Likewise, divergent transcription can be suppressed by targeting GRFs and TFs or the bulky dCas9 protein to transcriptional initiation sites. We propose that RSC mediated nucleosome positioning, GRFs including TFs form the physical barriers in promoters for limiting of divergent transcription, thereby controlling promoter directionality.
2021-07-27 | GSE179254 | GEO
Project description:Mammalian transcriptomes are complex and formed by extensive promoter activity. Moreover, gene promoters are largely divergent and initiate transcription of reverse-oriented promoter upstream transcripts (PROMPTs). Although PROMPTs are commonly terminated early, influenced by early polyadenylation (pA) sites, promoters often cluster so that the divergent activity of one might impact another. Here, we find that the distance between promoters strongly correlates with the expression, stability and length of their associated PROMPTs. Adjacent promoters driving divergent mRNA transcription support PROMPT formation, but due to pA site constraints, these transcripts tend to spread into the neighboring mRNA on the same strand. This mechanism to derive new alternative mRNA transcription start sites (TSSs) is also evident at closely spaced promoters supporting convergent mRNA transcription. We suggest that basic building blocks of divergently transcribed core promoter pairs, in combination with the wealth of TSSs in mammalian genomes, provides a framework with which evolution shapes transcriptomes.
2016-05-13 | GSE75183 | GEO
Project description:The directionality of gene promoters, the proportion of protein coding over divergent noncoding transcription, is highly variable and regulated. How promoter directionality is controlled remains poorly understood. We show that chromatin remodelling complex RSC, general regulatory factors (GRFs) including transcription factors (TFs) can facilitate promoter directionality by attenuating divergent noncoding transcription. Depletion of RSC increased divergent noncoding and decreased protein coding transcription of promoters with strong directionality. Consistent with RSC’s role in regulating chromatin, RSC depletion negatively impacts nucleosome positions upstream of the nucleosome depleted region where divergent transcription initiates, suggesting that nucleosome positioning upstream in promoters physically blocks the recruitment of transcription machinery. Likewise, divergent transcription can be suppressed by targeting GRFs and TFs or the bulky dCas9 protein to transcriptional initiation sites. We propose that RSC mediated nucleosome positioning, GRFs including TFs form the physical barriers in promoters for limiting of divergent transcription, thereby controlling promoter directionality.
2021-07-27 | GSE179255 | GEO