Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE81537
PROVIDER: PRJNA321872 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Uridylation-mediated RNA quality control pathway in mammalian cytoplasm [CLIP-Seq]
| PRJNA321870 | ENA
Project description:Uridylation of various cellular RNA species at the 3’ end has been generally linked to RNA degradation. Uridylated pre-miRNAs in mammals and uridylated mRNAs in fission yeast are targeted by the 3′ to 5′ exoribonuclease DIS3L2. In humans, DIS3L2 mutations have been associated with Perlman syndrome development and Wilms tumor susceptibility. In this work, we employ crosslinking in vivo and immunoprecipitation (CLIP) method to assess the RNA binding capacity of human DIS3L2 on a genome-wide scale. Our study uncovers a broad spectrum of uridylated RNAs in human cytoplasm, which include mature as well as aberrant forms of coding and noncoding RNAs, such as rRNAs, snRNAs, snoRNAs, tRNAs and pre-miRNAs. Most importantly, we have identified that a fraction of Pol II transcription start-site associated transcripts are exported to cytoplasm, where they are targeted by the TUT-DIS3L2 pathway. Moreover, this pathway appears to mainly target RNA regions that form stable secondary structures. Our findings imply the role of DIS3L2 and oligouridylation in general RNA quality control of most, if not all RNA classes.
2016-09-27 | GSE81536 | GEO
Project description:Uridylation of various cellular RNA species at the 3’ end has been generally linked to RNA degradation. Uridylated pre-miRNAs in mammals and uridylated mRNAs in fission yeast are targeted by the 3′ to 5′ exoribonuclease DIS3L2. In humans, DIS3L2 mutations have been associated with Perlman syndrome development and Wilms tumor susceptibility. In this work, we employ crosslinking in vivo and immunoprecipitation (CLIP) method to assess the RNA binding capacity of human DIS3L2 on a genome-wide scale. Our study uncovers a broad spectrum of uridylated RNAs in human cytoplasm, which include mature as well as aberrant forms of coding and noncoding RNAs, such as rRNAs, snRNAs, snoRNAs, tRNAs and pre-miRNAs. Most importantly, we have identified that a fraction of Pol II transcription start-site associated transcripts are exported to cytoplasm, where they are targeted by the TUT-DIS3L2 pathway. Moreover, this pathway appears to mainly target RNA regions that form stable secondary structures. Our findings imply the role of DIS3L2 and oligouridylation in general RNA quality control of most, if not all RNA classes.
2016-09-27 | GSE81534 | GEO
Project description:In the cytoplasm, small RNAs can control mammalian translation by regulating the stability of mRNA. In the nucleus, small RNAs can also control transcription and splicing. The mechanisms for RNA-mediated nuclear regulation are not understood and remain controversial, hindering the effective application of nuclear RNAi and blinding investigation of its natural regulatory roles. Here we reveal that the human GW182 paralogs TNRC6A/B/C are central organizing factors critical to RNA-mediated transcriptional activation. Mass spectrometry of purified nuclear lysates followed by experimental validation demonstrates that TNRC6A interacts with proteins involved in protein degradation, RNAi, the CCR4-NOT complex, the mediator complex, and histone modifying complexes. Functional analysis implicates TNRC6A, NAT10, MED14, and WDR5 in RNA-mediated transcriptional activation. These findings describe protein complexes capable of bridging RNA-mediated sequence-specific recognition of noncoding RNA transcripts with the regulation of gene transcription.
2017-07-07 | MSV000081227 | MassIVE
Project description:Mutations in the 3’-5’ exonuclease DIS3L2 are associated with Perlman syndrome and hypersusceptibility to Wilms’ tumorigenesis. Previously, we found that Dis3l2 specifically recognizes and degrades uridylated pre-let-7 microRNA. However, the widespread relevance of Dis3l2-mediated decay of uridylated substrates remains unknown. Here we applied an unbiased RNA immunoprecipitation strategy to identify Dis3l2 targets in mouse embryonic stem cells. The disease-associated long noncoding RNA (lncRNA) Rmrp, 7SL, as well as several other Pol III-transcribed noncoding RNAs (ncRNAs) were among the most highly enriched Dis3l2-bound RNAs. 3’-uridylated Rmrp, 7SL, and snRNA species were highly stabilized in the cytoplasm of Dis3l2-depleted cells. Deep sequencing analysis of Rmrp 3’ ends revealed extensive oligouridylation mainly on transcripts with imprecise ends. We implicate the TUTases Zcchc6/11 in the uridylation of these ncRNAs, and biochemical reconstitution assays demonstrate the sufficiency of TUTase-Dis3l2 for Rmrp decay. This establishes Dis3l2-Mediated Decay (DMD) as a quality control pathway that eliminates aberrant ncRNAs.obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells, neural progenitor cells and embryonic fibroblasts. We find that lysine 4 and lysine 27 trimethylation effectively discriminates genes that are expressed, poised for expression, or stably repressed, and therefore reflect cell state and lineage potential. Lysine 36 trimethylation marks primary coding and non-coding transcripts, facilitating gene annotation. Trimethylation of lysine 9 and lysine 20 is detected at satellite, telomeric and active long-terminal repeats, and can spread into proximal unique sequences. Lysine 4 and lysine 9 trimethylation marks imprinting control regions. Finally, we show that chromatin state can be read in an allele-specific manner by using single nucleotide polymorphisms. This study provides a framework for the application of comprehensive chromatin profiling towards characterization of diverse mammalian cell populations.
2016-07-08 | GSE84107 | GEO
Project description:Dis3l2-Mediated Decay Is a Quality Control Pathway for Noncoding RNAs
| PRJNA328029 | ENA
Project description:JunB control of keratinocyte-mediated inflammation [RNA-seq]
| PRJNA266557 | ENA
Project description:Small silencing RNAs are key regulators of gene expression in both plants and animals. HEN1-mediated 3’ terminal 2’-O-methylation plays a crucial role in small RNA stability control. In the absence of HEN1, small RNAs are frequently uridylated (untemplated uridine addition) and trimmed, a phenomenon that is conserved across species. However, the underlying molecular mechanism is largely unknown. In this study, we have discovered UTP: RNA uridylyltransferase (URT1) acts redundantly with HESO1 in the uridylation of miRNAs, in addition to its role in oligo-adenylated mRNA uridylation. We show both common and distinctive features of URT1 and HESO1 in catalyzing miRNA uridylation. non coding RNA deep sequencing
2015-07-01 | E-GEOD-60826 | biostudies-arrayexpress
Project description:Nonsense-mediated decay (NMD) is a translation-dependent RNA quality control mechanism that occurs in the cytoplasm. However, it is unknown how NMD regulates the stability of RNAs translated at the Endoplasmic Reticulum (ER). Here, we identify a localized NMD pathway dedicated to ER-translated mRNAs. We previously identified NBAS, a component of the Syntaxin 18 complex involved in Golgi-to-ER trafficking, as a novel NMD factor. Here, we show that NBAS fulfils an independent function in NMD. This ER-NMD pathway requires the interaction of NBAS with the core NMD factor UPF1, which is partially localized at the ER in the proximity of the translocon. NBAS and UPF1 co-regulate the stability of ER-associated transcripts, in particular those associated with the cellular stress response. We propose a model where NBAS recruits UPF1 to the membrane of the ER and activates an ER-dedicated NMD pathway, thus providing an ER protective function by ensuring quality control of ER-translated mRNAs.
2020-06-15 | GSE152436 | GEO
Project description:Nonsense-mediated decay (NMD) is a translation-dependent RNA quality control mechanism that occurs in the cytoplasm. However, it is unknown how NMD regulates the stability of RNAs translated at the Endoplasmic Reticulum (ER). Here, we identify a localized NMD pathway dedicated to ER-translated mRNAs. We previously identified NBAS, a component of the Syntaxin 18 complex involved in Golgi-to-ER trafficking, as a novel NMD factor. Here, we show that NBAS fulfils an independent function in NMD. This ER-NMD pathway requires the interaction of NBAS with the core NMD factor UPF1, which is partially localized at the ER in the proximity of the translocon. NBAS and UPF1 co-regulate the stability of ER-associated transcripts, in particular those associated with the cellular stress response. We propose a model where NBAS recruits UPF1 to the membrane of the ER and activates an ER-dedicated NMD pathway, thus providing an ER protective function by ensuring quality control of ER-translated mRNAs.
2020-06-15 | GSE152435 | GEO