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A strand-specific switch in noncoding transcription switches the function of a Polycomb/Trithorax response element

ABSTRACT: Polycomb/Trithorax response elements (PRE/TREs) can switch their function reversibly between silencing and activation, by mechanisms that are poorly understood. Here we show that a switch in forward and reverse noncoding transcription from the Drosophila vestigial (vg) PRE/TRE switches the status of the element between silencing (induced by the forward strand) and activation (induced by the reverse strand). In vitro, both ncRNAs inhibit PRC2 histone methyltransferase activity, but in vivo only the reverse strand binds PRC2. Overexpression of the reverse strand evicts PRC2 from chromatin and inhibits its enzymatic activity. We propose that interactions of RNAs with PRC2 are differentially regulated in vivo, allowing regulated inhibition of local PRC2 activity. Genome-wide analysis shows that strand switching of ncRNAs occurs at several hundred PcG binding sites in fly and vertebrate genomes. This work identifies a novel and potentially widespread class of PRE/TREs that switch function by switching the direction of ncRNA transcription.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE59192 | GEO | 2014/08/10

SECONDARY ACCESSION(S): PRJNA254705

REPOSITORIES: GEO

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A strand-specific switch in noncoding transcription switches the function of a Polycomb/Trithorax response element

Project description:Polycomb/Trithorax response elements (PRE/TREs) can switch their function reversibly between silencing and activation, by mechanisms that are poorly understood. Here we show that a switch in forward and reverse noncoding transcription from the Drosophila vestigial (vg) PRE/TRE switches the status of the element between silencing (induced by the forward strand) and activation (induced by the reverse strand). In vitro, both ncRNAs inhibit PRC2 histone methyltransferase activity, but in vivo only the reverse strand binds PRC2. Overexpression of the reverse strand evicts PRC2 from chromatin and inhibits its enzymatic activity. We propose that interactions of RNAs with PRC2 are differentially regulated in vivo, allowing regulated inhibition of local PRC2 activity. Genome-wide analysis shows that strand switching of ncRNAs occurs at several hundred PcG binding sites in fly and vertebrate genomes. This work identifies a novel and potentially widespread class of PRE/TREs that switch function by switching the direction of ncRNA transcription. E(Z) and H3K27me3 profile in Drosophila embryos of two transgenic lines (pKC27.vg.fwd' and pKC27.vg.rev') that were crossed to daGAL4 in order to overexpress the forward or the reverse vg PRE/TRE ncRNA from an ectopic site ('site 1' in this study).

2014-08-10 | E-GEOD-59192 | biostudies-arrayexpress

A mechanism for microRNA arm switching regulated by uridylation [AQ-seq]

Project description:Strand selection is a critical step in microRNA (miRNA) biogenesis. Although the dominant strand may alter depending on cellular contexts, the molecular mechanism and physiological significance of such alternative strand selection (or “arm switching”) remain elusive. Here we find miR-324 as one of the strongly regulated miRNAs by arm switching, and identify terminal uridylyl transferases TUT4 and TUT7 as the key regulators. Uridylation of pre-miR-324 by TUT4/7 re-positions DICER on the pre-miRNA and shifts the cleavage site. This alternative processing produces a duplex with a different terminus, from which the 3′ strand (3p) is selected instead of the 5′ strand (5p). In glioblastoma, the TUT4/7 and 3p levels are upregulated while the 5p level is reduced. Manipulation of the strand ratio is sufficient to impair glioblastoma cell proliferation. This study uncovers a role of uridylation as a molecular switch in alternative strand selection and implicates its therapeutic potential.

2020-04-15 | GSE148686 | GEO

A mechanism for microRNA arm switching regulated by uridylation [RNA-seq]

2020-04-15 | GSE148685 | GEO

Re-analysis of E-MTAB-1585

Project description:Raw data from E-MTAB-1585 was normalized by using reads per million. https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1585/ Strand specific RNA-Seq data E-MTAB-1585 was normalized and subtracted control from knockdown to generate tracks that more clearly displayed the unusual pattern of RNA expression caused by knockdown of 7SK. The following wig files were generated from multiple samples (i.e.raw data files), as indicated in the 'readme.txt' file. 7sk_3p_KD_norm.wig: 7SK 3P Knockdown normalized 7sk_3p_KDF_norm.wig: 7SK 3P Knockdown normalized (Forward) 7sk_3p_KDR_norm.wig: 7SK 3P Knockdown normalized (Reverse) 7sk_5p_KD_norm.wig: 7SK 5P Knockdown normalized 7sk_5p_KDF_norm.wig: 7SK 5P Knockdown normalized (Forward) 7sk_5p_KDR_norm.wig: 7SK 5P Knockdown normalized (Reverse) 7sk_Control_norm.wig: 7SK Control normalized 7sk_ControlF_norm.wig: 7SK Control normalized (Forward) 7sk_ControlR_norm.wig: 7SK Control normalized (Reverse) 7sk_3p_KDF-ControlF.wig: 7SK 3P Knockdown-Control (Forward) 7sk_3p_KDR-ControlR.wig: 7SK 3P Knockdown-Control (Reverse) 7sk_5p_KDF-ControlF.wig: 7SK 5P Knockdown-Control (Forward) 7sk_5p_KDR-ControlR.wig: 7SK 5P Knockdown-Control (Reverse)

2013-09-19 | E-GEOD-50860 | biostudies-arrayexpress

Template switching by a group II intron reverse transcriptase: biochemical analysis and implications for RNA-seq

Project description:The reverse transcriptases (RTs) encoded by mobile group II intron and other non-LTR-retro-elements differ from retroviral RTs in being able to template switch from the 5' end of one template to the 3' end of another without pre-existing complementarity between the donor and acceptor nucleic acids. Here, we used the ability of a thermostable group II intron RT (TGIRT) to template switch directly from synthetic RNA template/DNA primer duplexes having either a blunt end or a 3'-DNA overhang end to establish a complete kinetic framework for the reaction and identify conditions that more efficiently capture acceptor RNAs or DNAs. The rate and amplitude of template switching are optimal from starter duplexes with a single nucleotide 3'-DNA overhang complementary to the 3' nucleotide of the acceptor RNA, suggesting a role for non-templated nucleotide addition of a complementary nucleotide to the 3’ end of cDNAs synthesized from natural templates. Longer 3'-DNA overhangs progressively decrease the rate of template switching, even when complementary to the 3' end of the acceptor template. Although dependent upon only a single base pair between the donor and acceptor, template switching discriminates against mismatches, which coupled with the high processivity of the enzyme, enables the synthesis of full-length DNA copies of acceptor nucleic acids beginning directly at their 3' end. We discuss possible biological functions of the template-switching activity of group II intron and other non-LTR-retroelements RTs, as well as the optimization of this activity for adapter addition in RNA-and DNA-seq.

2019-11-11 | GSE138200 | GEO

Characterization of Arabidopsis thaliana promoter bidirectionality and antisense RNAs by depletion of nuclear RNA decay pathways

Project description:In animals, transcription by RNA polymerase II initiates bidirectionally from gene promoters to produce pre-mRNAs on the forward strand and promoter upstream transcripts (PROMPTs) on the reverse strand. PROMPTs are rapidly degraded by the nuclear exosome. Previous studies based on nascent RNA approaches concluded that Arabidopsis thaliana does not produce PROMPTs. Here, we used steady-state RNA sequencing methods in mutants defective in nuclear RNA decay, including by the exosome, to reassess the existence of PROMPTs in A. thaliana. While PROMPTs are overall rare in A. thaliana, about 100 clear cases of exosome-sensitive PROMPTs were identified. We also found that PROMPTs become sources of 21-22 nt small interfering RNAs in exosome-deficient mutants, perhaps explaining why plants have evolved mechanisms to suppress PROMPT production. In addition, we found ~200 transcription start sites within 3’-UTR-encoding regions that produce long unspliced, exosome-sensitive antisense RNAs. The previously characterized non-coding (nc) RNA that regulates expression of the key seed dormancy regulator, DELAY OF GERMINATION1, is a typical representative of this class of RNAs. Transcription factor genes are overrepresented among loci with exosome-sensitive antisense RNAs, suggesting a potential for widespread control of gene expression via this class of ncRNAs. Lastly, we assess the use of alternative promoters in A. thaliana and compare the accuracy of existing TSS annotations.

2020-02-17 | GSE142555 | GEO

Characterization of Arabidopsis thaliana promoter bidirectionality and antisense RNAs by depletion of nuclear RNA decay pathways [CAGE-seq]

2020-02-17 | GSE136356 | GEO

Characterization of Arabidopsis thaliana promoter bidirectionality and antisense RNAs by depletion of nuclear RNA decay pathways [RNA-seq]

2020-02-17 | GSE136362 | GEO

Molecular Profiling of Cancer

Project description:<p>Noncoding RNAs (ncRNAs) are emerging as key molecules in human cancer, with the potential to serve as novel markers of disease and to reveal uncharacterized aspects of tumor biology. Here we discover 121 unannotated prostate cancer-associated ncRNA transcripts (PCATs) by <i>ab initio</i> assembly of high-throughput sequencing of polyA+ RNA (RNA-Seq) from a cohort of 102 prostate tissues and cells lines. We characterized one ncRNA, PCAT-1, as a prostate-specific regulator of cell proliferation and show that it is a target of the polycomb repressive complex 2 (PRC2). We further found that patterns of PCAT-1 and PRC2 expression stratified patient tissues into molecular subtypes distinguished by expression signatures of PCAT-1-repressed target genes. Taken together, our findings suggest that PCAT-1 is a transcriptional repressor implicated in a subset of prostate cancer patients. These findings establish the utility of RNA-Seq to identify disease-associated ncRNAs that may improve the stratification of cancer subtypes.</p>

| phs000443 | dbGaP

KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells

Project description:Vascular smooth muscle cells (VSMCs) within atherosclerotic lesions undergo a phenotypic switching in a KLF4-dependent manner. Glycolysis plays important roles in transdifferentiation of somatic cells, however, it is unclear whether and how KLF4 mediates the link between glycolytic switch and VSMCs phenotypic transitions. Here, we show that KLF4 upregulation accompanies VSMCs phenotypic switching in atherosclerotic lesions. KLF4 enhances the metabolic switch to glycolysis through increasing PFKFB3 expression. Inhibiting glycolysis suppresses KLF4-induced VSMCs phenotypic switching, demonstrating that glycolytic shift is required for VSMCs phenotypic switching. Mechanistically, KLF4 upregulates expression of circCTDP1 and eEF1A2, both of which cooperatively promote PFKFB3 expression. TMAO induces glycolytic shift and VSMCs phenotypic switching by upregulating KLF4. Our study indicates that KLF4 mediates the link between glycolytic switch and VSMCs phenotypic transitions, suggesting that a previously unrecognized KLF4-eEF1A2/circCTDP1-PFKFB3 axis plays crucial roles in VSMCs phenotypic switching.

2022-11-09 | PXD038057 | iProX

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