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Shape of promoter antisense RNAs regulates ligand-induced transcription activation [Shape-Map]

ABSTRACT: Shape of promoter antisense RNAs regulates ligand-induced transcription activation [Shape-Map]

PROVIDER: PRJNA686387 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13272471_1.fastq.gz	Fastqsanger.gz
	SRR13272471_2.fastq.gz	Fastqsanger.gz
	SRR13272472_1.fastq.gz	Fastqsanger.gz
	SRR13272472_2.fastq.gz	Fastqsanger.gz
	SRR13272473_1.fastq.gz	Fastqsanger.gz

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Shape of promoter antisense RNAs regulates ligand-induced transcription activation

Project description:Shape of promoter antisense RNAs regulates ligand-induced transcription activation

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Shape of promoter antisense RNAs regulates ligand-induced transcription activation [Shape-Map]

Project description:Demonstration of a massive lncRNA RNA transcriptional program in the mammalian genome has engendered lively discussions about their biological roles, particularly the promoter antisense (PAS) transcripts of coding gene transcription units and abundant species localized to specific subnuclear structures with phase separation properties. Here, we report development of an alternative assay to quantitatively detect RNA distribution in the genome, referred to as ChIRC-seq (Chromatin Isolation by RNA-Cas13a Complex Capture by Cas13a), which has revealed that promoter antisense RNAs (PAS-RNAs) serve as a key gatekeeper of a broad transcriptional pause release program, based on decommissioning the 7SK snRNA-dependent inhibitory P-TEFb complex. Induction of PAS-RNA by liganded estrogen receptor ERα (ESR1) releases the basal recruitment of HP1α and KAP1 on target gene promoters, without the spreading characteristic of extended heterochromatic regions, based on PAS-dependent recruitment of H3K9me3 demethylases. Unexpectedly, ERα-bound MegaTrans enhancer activation with features of phase separation events proved to require recruitment of phosphorylated KAP1 to be activated, with its transfer to the cognate promoters licensing estrogen-induced pause release and target gene activation. The ChIRC13a-seq method has proved effective for identification of the cognate promoter for activated enhancers and has revealed that the lncRNAs NEAT1/MALAT1 in phase-separated subnuclear structures interact with robust estrogen-activated MegaTrans TFF1e1 enhancer and other active enhancers, linking acute activation of a subset of enhancers to interactions with specific phase-separated subnuclear architectural structures.

2021-03-24 | GSE163494 | GEO

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Shape of promoter antisense RNAs regulates ligand-induced transcription activation.

Project description:The size of the transcriptional program of long non-coding RNAs in the mammalian genome has engendered discussions about their biological roles1, particularly the promoter antisense (PAS) transcripts2,3. Here we report the development of an assay-referred to as chromatin isolation by RNA-Cas13a complex-to quantitatively detect the distribution of RNA in the genome. The assay revealed that PAS RNAs serve as a key gatekeeper of a broad transcriptional pause release program, based on decommissioning the 7SK small nuclear RNA-dependent inhibitory P-TEFb complex. Induction of PAS RNAs by liganded ERα led to a significant loss of H3K9me3 and the release of basally recruited HP1α and KAP1 on activated target gene promoters. This release was due to PAS RNA-dependent recruitment of H3K9me3 demethylases, which required interactions with a compact stem-loop structure in the PAS RNAs, an apparent feature of similarly regulated PAS RNAs. Activation of the ERα-bound MegaTrans enhancer, which is essential for robust pause release, required the recruitment of phosphorylated KAP1, with its transfer to the cognate promoters permitting 17β-oestradiol-induced pause release and activation of the target gene. This study reveals a mechanism, based on RNA structure, that mediates the function of PAS RNAs in gene regulation.

| S-EPMC8439151 | biostudies-literature

Shape of promoter antisense RNAs regulates ligand-induced transcription activation

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

2021-03-24 | GSE139199 | GEO

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Antisense lncRNA transcription mediates DNA demethylation to drive stochastic Protocadherin α promoter choice

Project description:Stochastic activation of clustered Protocadherin (Pcdh) α, β, and γ genes generates a cell-surface identity code in individual neurons that functions in neural circuit assembly. Here, we show that Pcdhα gene choice involves the activation of an antisense promoter located in the first exon of each Pcdhα alternate gene. Transcription of an antisense long noncoding RNA (lncRNA) from this antisense promoter extends through the sense promoter, leading to DNA demethylation of the CTCF binding sites proximal to each promoter. Demethylation-dependent CTCF binding to both promoters facilitates cohesin-mediated DNA looping with a distal enhancer (HS5-1), locking in the transcriptional state of the chosen Pcdhα gene. Uncoupling DNA demethylation from antisense transcription by Tet3 overexpression in mouse olfactory neurons promotes CTCF binding to all Pcdhα promoters, resulting in proximity-biased DNA looping of the HS5-1 enhancer. Thus, antisense transcription-mediated promoter demethylation functions as a mechanism for distance-independent enhancer/promoter DNA looping to ensure stochastic Pcdhα promoter choice.

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