Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homotypic clustering of L1 and B1 repeats organizes 3D genome

ABSTRACT: We postulated that the primary DNA sequences, particularly abundant repetitive elements embedded in the genome, may instruct genome folding. Short and long interspersed nuclear elements (SINEs and LINEs, respectively) are two predominant sub-families of retrotransposons in most mammals. LINE-1 (LINE1 or L1) constitutes the most abundant type of repeat subclasses, making up to 18.8% and 17% (0.9~1.0 million copies) of the genome in mouse and human, respectively. B1 in mouse and its closely related, primate-specific Alu elements in human are the most abundant subclass of SINEs, constituting 2.7%~10% (0.6~1.4 million copies) of mouse and human genomes. Here, we demonstrate that B1/Alu and L1 repeats demarcate the genome into the A/B compartments and serve as the blueprint for the three-dimensional (3D) organization of mammalian genomes. Our finding explains the robustness and evolutionary conservation of nuclear chromatin organization in mammals. H3K9me3 ChIP-seq upon L1 AMO treatment; We electrotransfected L1 AMO into mESC to block L1 transcripts for 36 h and a standard control from GenTools was used as control -"SCR". We performed H3K9me3 ChIP-seq in mESCs treated with L1 or SCR AMO for 36 h. We found that L1 AMO did not alter the genome-wide binding of H3K9me3, ruling out the possibility that the loss of organization relates to changes in local heterochromatin marks.

ORGANISM(S): Mus musculus

PROVIDER: GSE123806 | GEO | 2020/12/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Growth signals employ CGGBP1 to suppress transcription of Alu-SINEs [Affymetrix]

Project description:Alu SINEs are the most numerous frequently occurring transcription units in our genome and possess sequence competence for transcription by RNA Pol III. However, through poorly understood mechanisms, the Alu RNA levels are maintained at very low levels in normal somatic cells with obvious benefits of low rates of Alu retrotransposition and energy-economical deployment of RNA Pol III to the tRNA genes which share promoter structure and polymerase requirements with Alu SINEs. Using comparative ChIP sequencing, we unveil that a repeat binding protein, CGGBP1, binds to the transcriptional regulatory regions of Alu SINEs thereby impeding Alu transcription by inhibiting RNA Pol III recruitment. We show that this Alu-silencing depends on growth factor stimulation of cells and subsequent tyrosine phosphorylation of CGGBP1. Importantly, CGGBP1 ensures a sequence-specific discriminative inhibition of RNA Pol III activity at Alu promoters, while sparing the structurally similar tRNA promoters. Our data suggest that CGGBP1 contributes to growth-related transcription by preventing the hijacking of RNA Pol III by Alu SINEs. This study was used to find out the effect of CGGBP1 on serum-induced changes in gene expression and effect of serum on gene expression regulation by CGGBP1. Gene expression profiling of normal human fibroblasts under 4 different experimental perturbations: serum starvation or serum stimulation and CGGBP1 depletion or normal CGGBP1 levels.

2015-12-21 | E-GEOD-54058 | biostudies-arrayexpress

Growth signals employ CGGBP1 to suppress transcription of Alu-SINEs [ChIP-Seq]

Project description:Alu SINEs are the most numerous frequently occurring transcription units in our genomes and possess sequence competence for transcription by RNA Pol III. However, through poorly understood mechanisms, the Alu RNA levels are maintained at very low levels in normal somatic cells with obvious benefits of low rates of Alu retrotransposition and energy-economical deployment of RNA Pol III to the tRNA genes which share promoter structure and polymerase requirements with Alu SINEs. Using comparative ChIP sequencing, we unveil that a repeat binding protein, CGGBP1, binds to the transcriptional regulatory regions of Alu SINEs thereby impeding Alu transcription by inhibiting RNA Pol III recruitment. We show that this Alu-silencing depends on growth factor stimulation of cells and subsequent tyrosine phosphorylation of CGGBP1. Importantly, CGGBP1 ensures a sequence-specific discriminative inhibition of RNA Pol III activity at Alu promoters, while sparing the structurally similar tRNA promoters. Our data suggest that CGGBP1 contributes to growth-related transcription by preventing the hijacking of RNA Pol III by Alu SINEs. Examination of one DNA binding protein in two different conditions of treatment.

2015-04-29 | E-GEOD-53571 | biostudies-arrayexpress

B2 and ALU retrotransposons are self-cleaving RNAs whose activity is enhanced by EZH2

Project description:More than 98% of the mammalian genome is noncoding and approximately half is made up of transposable elements. One of the most abundant is the short interspersed nuclear elements (SINE). Among the million copies of SINEs, B2 accounts for ~350,000 in the mouse genome and have garnered special interest because of emerging roles in gene regulation. Our recent work demonstrated that B2 RNA normally binds stress genes to retard transcription elongation. Though epigenetically silenced, B2s become massively upregulated during thermal stress. Specifically, an interaction between B2 RNA and the Polycomb protein, EZH2, results in cleavage of B2 RNA, release of B2 RNA from RNA Polymerase II, and activation of the stress genes. Although an established RNA-binding protein and histone methyltransferase, EZH2 is not known to be a nuclease. Here, we provide evidence for the surprising conclusion that B2 is a self-cleaving RNA. Contact with EZH2 accelerates cleavage rate by >100-fold, suggesting that EZH2 may assist cleavage as an RNA chaperone. Modification-interference analysis demonstrate that phosphorothioate changes at A and C nucleotides can substitute for EZH2’s function. B2 mutagenesis indicate that nucleotides around positions 45-55 and 100-101 are critical for cleavage reaction. Finally, we demonstrate that another family of SINEs, the ALU elements produce also a self-cleaving RNA. ALUs are intrinsically more auto-reactive than B2s. We propose that the B2/ALU SINEs are a new class of ribozymes whose activity is accelerated by EZH2.

2020-01-31 | GSE139931 | GEO

Growth signals employ CGGBP1 to suppress transcription of Alu-SINEs [Affymetrix]

2015-12-21 | GSE54058 | GEO

Growth signals employ CGGBP1 to suppress transcription of Alu-SINEs [ChIP-Seq]

2015-04-29 | GSE53571 | GEO

LINE1 TGS mechanism mediated by SETDB1-AGO2 complex in human somatic cells [small RNA-seq]

Project description:LINE1s are abundant retroelements comprising 17% of human genome. Naturally, genomic LINE1s are tightly repressed by epigenetic mechanism; however, if relieved, they can be detrimental to genome stability by their transposition capability. So, a supervising mechanism that quickly re-represses the leaky LINE1s is demanded. Here we show that de-repressed LINE1s generate small RNAs, L1-siRNAs, which SETDB1 and AGO2 recognize, then move into searching for a transcript with sequence complementarity, and ultimately re-install a repression mechanism at LINE1 5’-untranslated region (5’UTR) by depositing trimethyl-H3K9 (H3K9me3). Immunoprecipitation (IP) results showed that SETDB1, AGO2, and L1-siRNA bound to each other and Chromatin-IP-seq and small-RNA-seq results demonstrated that they sat at the same locus within the 5’UTR. SETDB1, AGO2, and L1-siRNA all were necessary for LINE1 repression, particularly the evolutionary young and transposition-competent families such as L1HS/L1PA1 and L1PA2. KAP1, which frequently partners with SETDB1 for silencing local chromatin, was dispensible for the repression of young L1PAs. Our findings indicate that, as a surveillance mechanism, the L1-siRNA-triggered, SETDB1-AGO2-effected repair of epigenetic errors at the 5’UTR establishes a homeostatic re-repression mechanism on inadvertently de-repressed LINE1 copies over the genome.

2023-08-21 | GSE203288 | GEO

LINE1 TGS mechanism mediated by SETDB1-AGO2 complex in human somatic cells [MBD-seq]

2023-08-21 | GSE203286 | GEO

LINE1 TGS mechanism mediated by SETDB1-AGO2 complex in human somatic cells [ChIP-seq]

2023-08-21 | GSE203285 | GEO

LINE1 TGS mechanism mediated by SETDB1-AGO2 complex in human somatic cells [RNA-seq]

2023-08-21 | GSE203287 | GEO

SINE transcription by RNA polymerase III is suppressed by histone methylation but not DNA methylation

Project description:Nearly half the human genome is comprised of repetitive DNA, including short interspersed nuclear elements (SINEs) such as Alu. SINEs spread by retrotransposition, which requires their transcripts to be copied into DNA and then inserted into new chromosomal sites. This can lead to genetic damage through insertional mutagenesis and through chromosomal rearrangements between nonallelic SINEs at distinct loci. SINE DNA is heavily methylated and this is thought to suppress its accessibility and transcription, thereby protecting against retrotransposition. However, we provide several lines of evidence that methylated SINE DNA is occupied genome-wide by RNA polymerase III, including the use of high-throughput bisulphite sequencing of ChIP DNA (ChIP-BS-Seq). Loss of DNA methylation has little effect on expression of SINEs or their accessibility to transcription machinery. We present evidence that methylation of histones rather than DNA plays a dominant role in suppressing SINE expression.

2015-03-23 | GSE38794 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data