Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24296028_1.fastq.gz | Fastqsanger.gz | |||
| SRR24296028_2.fastq.gz | Fastqsanger.gz | |||
| SRR24296029_1.fastq.gz | Fastqsanger.gz | |||
| SRR24296029_2.fastq.gz | Fastqsanger.gz | |||
| SRR24296030_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:We characterize the TERRA transcriptome at normal and TRF2-depleted telomeres by RNA-seq and we demonstrate that TERRA upregulation is occurring at all transcribed telomeres upon depletion of TRF2. RNA-sequencing of HeLa mRNA, 4 samples: with or without TERRA enrichment by IP (respectively "IP" and "input"), with or without TFR-2 knock-down (respectively "_T" and "_EV").
2014-10-31 | E-GEOD-56727 | biostudies-arrayexpress
Project description:Through an integration of genomic and proteomic approaches to advance understanding of long noncoding RNAs, we investigate the function of the telomeric transcript, TERRA. By identifying thousands of TERRA target sites in the mouse genome, we demonstrate that TERRA can bind both in cis to telomeres and in trans to genic targets. We then define a large network of interacting proteins, including epigenetic factors, telomeric proteins, and the RNA helicase, ATRX. TERRA and ATRX share hundreds of target genes and are functionally antagonistic at these loci: whereas TERRA activates, ATRX represses gene expression. At telomeres, TERRA competes with telomeric DNA for ATRX binding, suppresses ATRX localization, and ensures telomeric stability. Depleting TERRA increases telomerase activity and induces telomeric pathologies, including formation of telomere-induced DNA damage foci and loss or duplication of telomeric sequences. We conclude that TERRA functions as an epigenomic modulator in trans and as an essential regulator of telomeres in cis.
2017-06-29 | GSE79180 | GEO
Project description:The genome consists of non-B-DNA structures such as G-quadruplexes (G4) that are involved in the regulation of genome stability and transcription. Telomeric-repeat containing RNA (TERRA) is capable of folding into G-quadruplex and interacting with chromatin remodeler ATRX. Here we show that TERRA modulates ATRX occupancy on repetitive sequences and over genes, and maintains DNA G-quadruplex structures at TERRA target and non-target sites in mouse embryonic stem cells. TERRA prevents ATRX from binding to subtelomeric regions and represses H3K9me3 formation. G4 ChIP-seq reveals that G4 abundance decreases at accessible chromatin regions, particularly at transcription start sites (TSS) after TERRA depletion; such G4 reduction at TSS is associated with elevated ATRX occupancy and differentially expressed genes. Loss of ATRX alleviates the effect of gene repression caused by TERRA depletion. Immunostaining analyses demonstrate that knockdown of TERRA diminishes DNA G4 signals, whereas silencing ATRX elevates G4 formation. Our results uncover an epigenetic regulation by TERRA that sequesters ATRX and preserves DNA G4 structures.
2022-11-09 | GSE194038 | GEO
Project description:We characterize the TERRA transcriptome at normal and TRF2-depleted telomeres by RNA-seq and we demonstrate that TERRA upregulation is occurring at all transcribed telomeres upon depletion of TRF2.
2014-10-31 | GSE56727 | GEO
Project description:In mammals, homologous chromosomes rarely pair outside meiosis. One exception is the X chromosome, which transiently pairs during X-chromosome inactivation (XCI). How two chromosomes find each other in 3D space is not known. Here, we reveal a required interaction between the X-inactivation center (Xic) and the telomere in mouse embryonic stem (ES) cells. The subtelomeric, pseudoautosomal regions (PARs) of the two sex chromosomes (X and Y) also undergo pairing in both female and male cells. PARs transcribe a class of telomeric RNA, dubbed PAR-TERRA, which accounts for a vast majority of all TERRA transcripts. PAR-TERRA binds throughout the genome, including to the PAR and Xic. During X-chromosome pairing, PAR-TERRA anchors the Xic to the PAR, creating a ‘tetrad’ of pairwise homologous interactions (Xic–Xic, PAR–PAR, and Xic–PAR). Xic pairing occurs within the tetrad. Depleting PAR-TERRA abrogates pairing and blocks initiation of XCI, whereas autosomal PAR-TERRA induces ectopic pairing. We propose a ‘constrained diffusion model’ in which PAR-TERRA creates an interaction hub to guide Xic homology searching during XCI.
2017-07-10 | GSE69887 | GEO
Project description:The tumor microenvironment is essential for cancer progression, yet the nuclear mechanisms that reprogram stromal fibroblasts into cancer-associated fibroblasts (CAFs) remain to be defined. Here, we identify a telomere-derived RNA–protein signaling axis that links genome integrity and fibroblast plasticity. We show that the long non-coding RNA TERRA, transcribed from telomeres, is upregulated in CAFs across multiple human skin cancers following loss of androgen receptor (AR) expression. Elevated TERRA enhances telomeric DNA damage and activates a CAF-specific transcriptional program. Through proteomic profiling, we identify the RNA-binding protein NONO as a critical TERRA effector. TERRA and NONO form nuclear complexes selectively in CAFs, while in normal fibroblasts NONO associates with AR. Disruption of the TERRA-NONO complex, either by genetic silencing or a small-molecule inhibitor of NONO, reverses CAF activation and suppresses tumor-stroma cells expansion in vitro and in vivo. These findings uncover a telomere-encoded mechanism of stromal reprogramming and identify the TERRA–NONO complex as a targetable point of vulnerability in the tumor microenvironment.
2026-08-10 | GSE300353 | GEO