Shape of promoter antisense RNAs regulates ligand-induced transcription activation [Shape-Map]
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PROVIDER: PRJNA686387 | ENA |
REPOSITORIES: ENA
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Project description:Shape of promoter antisense RNAs regulates ligand-induced transcription activation
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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.
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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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Project description:RNA secondary structure is crucial for RNA mentalism, including transcription, splicing, translation, RNA-binding protein interaction as well as turnover. The kink-turn (K-turn) structure motif is is an RNA three-dimensional (3D) structure that exists in all three primary phylogenetic domains and plays vital roles in RNA metabolism. In order to investigate the K-turn secondary structure in vivo, we combined SHAPE-Map and our RIP-PEN-seq to profile the RNA structure of 15.5K-interacted RNAs.
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Project description:The capacity of cells to retain a memory of previous signals enables them to adopt unique cell fates and adjust to their surrounding environment. The underlying gene expression memory can arise from mutual repression of two genes, forming a toggle switch. Such mutual repression may occur at antisense loci, where two convergently oriented genes repress each other in cis. Under which conditions antisense transcription can generate expression memory remains poorly understood. To address this question, we combine mathematical modeling, genomics and a synthetic biology approach. Through simulations we show that stable memory can emerge, if both genes in an antisense pair transcribe through the convergent promoter and induce a stable repressive chromatin state. Genome-wide analysis of nascent transcription further supports antisense-mediated promoter repression with promoter-overlapping antisense gene pairs exhibiting mutually exclusive expression. Through constructing a synthetic antisense locus in mouse embryonic stem cells (mESCs) we then show that such a locus architecture can indeed maintain a memory of a transient stimulus. Mutual repression and the capacity for memory formation are elevated, when mESCs differentiate, showing that epigenetic memory is a cell type-specific property. Our finding that stem cells adapt their ability to remember stimuli as they differentiate might help to elucidate how stemness is maintained.
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Project description:RNA polymerase II and PARP1 shape enhancer-promoter contacts
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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 | GSE139196 | GEO