Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transfer RNA (tRNA) processing profiles of mouse embryonic frontal lobes at E13.5/E18.5

ABSTRACT: Purpose: High-throughput RNA sequencing has accelerated discovery of the complex regulatory roles of small RNAs, such those derived from tRNAs. Also recent advances in high-throughput RNA sequencing has revealed the complex RNA modification landscape and the complex role these nucleosides modifactions have in cell signalling, stem cell biology and development. The goal of this study is to establish how tRNA-derived small RNAs can affect stem cell function. Methods: four replicates of tRNAs sequencing of wild-type (WT) and NSun2 -/- mouse embryonic frontal lobes at E18.5 were generated by deep sequencing, using Illumina HiSeq platform. Results: Our analyses reveal that deletion of the cytosine-5 tRNA methylase NSUN2 increases tRNA cleaveage of NSUN2 tRNA substrates.

ORGANISM(S): Mus musculus

PROVIDER: GSE82162 | GEO | 2017/01/02

SECONDARY ACCESSION(S): PRJNA324234

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transfer RNA (tRNA) processing and RNA m5C-methylation profiles of mouse skin squamous tumours

Project description:Purpose: High-throughput RNA sequencing has accelerated discovery of the complex regulatory roles of small RNAs, such those derived from tRNAs. Also recent advances in high-throughput RNA sequencing has revealed the complex RNA modification landscape and the complex role these nucleosides modifactions have in cell signalling, stem cell biology, development and cancer. The goal of this study is to establish how m5C-tRNA methylation and tRNA-derived small RNAs can affect stem cell fucntion in cancer. Methods: four replicates of tRNAs and RNA buisulphite sequencing of wild-type (WT) and NSun2 -/- mouse skin squamous tumours were generated by deep sequencing, using Illumina HiSeq platform. Results: Our analyses reveal that inhibition of post-transcriptional cytosine-5 methylation locks stem cells in this distinct translational inhibition programme that results in tumour progression but that also sentizes cancer cells to genotoxic stress. Transfer RNA (tRNA) sequencing and RNA Bisulphite sequencing of wild-type (WT) and NSun2 -/- mouse skin squamous tumours

2016-06-16 | E-GEOD-72065 | biostudies-arrayexpress

Transfer RNA (tRNA) processing and RNA m5C-methylation profiles of mouse skin squamous tumours

2016-06-16 | GSE72065 | GEO

Loss of cytosine-5 methylation in tRNA triggers stress responses in a disease model for Intellectual Disability

Project description:Mutations in the cytosine-5 RNA methyltransferase NSun2 can cause Intellectual Disability (ID) and symptoms commonly found in patients with Dubowitz syndrome. By analysing gene expression data with the global cytosine-5 RNA methylome in NSun2-deficient mice, we find that loss of cytosine-5 RNA methylation increases the fragmentation of transfer RNAs (tRNA) leading to an accumulation of 5M-bM-^@M-^Y halves. Cleavage of tRNAs by Angiogenin is a common cellular stress response to silence translational programmes, and we show that Angiogenin binds tRNAs lacking site-specific NSun2-methylation with higher affinity. Furthermore, cells lacking functional NSun2 up-regulate stress markers, and deletion of NSun2 compromises cellular survival in response stress stimuli including UV-light and oxidative stress. The decreased tolerance of NSun2 null cells towards oxidative stress can be rescued through inhibition of Angiogenin. In conclusion, cytosine-5 RNA methylation is an essential post-transcriptional mechanism during cellular stress responses and NSun2-mediated tRNA methylation protects from Angiogenin-dependent stress-induced RNA cleavage. RNA Methylation profiling by high throughput sequencing small non-coding RNA profiling by high throughput sequencing Pol III Chromatin-IP profiling by high throughput sequencing

2014-11-06 | E-GEOD-44746 | biostudies-arrayexpress

Loss of cytosine-5 methylation in tRNA triggers stress responses in a disease model for Intellectual Disability

Project description:Mutations in the cytosine-5 RNA methyltransferase NSun2 can cause Intellectual Disability (ID) and symptoms commonly found in patients with Dubowitz syndrome. By analysing gene expression data with the global cytosine-5 RNA methylome in NSun2-deficient mice, we find that loss of cytosine-5 RNA methylation increases the fragmentation of transfer RNAs (tRNA) leading to an accumulation of 5’ halves. Cleavage of tRNAs by Angiogenin is a common cellular stress response to silence translational programmes, and we show that Angiogenin binds tRNAs lacking site-specific NSun2-methylation with higher affinity. Furthermore, cells lacking functional NSun2 up-regulate stress markers, and deletion of NSun2 compromises cellular survival in response stress stimuli including UV-light and oxidative stress. The decreased tolerance of NSun2 null cells towards oxidative stress can be rescued through inhibition of Angiogenin. In conclusion, cytosine-5 RNA methylation is an essential post-transcriptional mechanism during cellular stress responses and NSun2-mediated tRNA methylation protects from Angiogenin-dependent stress-induced RNA cleavage.

2014-11-06 | GSE44746 | GEO

tRNA gene identity acts as a determinant of gene positioning

Project description:Here we report that the spatial organization of yeast tRNA genes depends upon both locus position and tRNA identity; supporting the idea that the genomic organization of tRNA loci utilizes tRNA dependent signals within the nucleoprotein-tRNA complexes that form into clusters. We use high-throughput sequencing coupled to Circular Chromosome Conformation Capture to detect interactions with two wild type tRNAs and these same positions replaced with suppressor tRNAs (SUP4-1). Detect DNA-DNA interactions (Circular chromosome conformation capture; 4C) with two wild type tRNAs and these same positions replaced with suppressor tRNAs (SUP4-1) Supplementary files: Alignment files generated by Topography v1.19 software.

2012-06-13 | E-GEOD-30103 | biostudies-arrayexpress

Neuronal Nsun2 deficiency is associated with codon-specific epitranscriptomic dysregulation of Gly-tRNAs and corresponding proteomic shift impacting synaptic signaling and behavior

Project description:Epitranscriptomic mechanisms linking the brain proteome to cognition and complex behaviors essentially remain unexplored. Here, we describe bi-directional changes in depression-related behaviors after genetic disruption of neuronal tRNA cytosine methylation, including conditional ablation and transgene-derived overexpression of NOL1/NOP2/SUN domain 2 (Nsun2) in the prefrontal cortex (PFC). Neuronal Nsun2-deficiency was associated with a sharp drop in tRNA m5C levels, resulting in significant deficits in expression of 70% (7/10) of tRNAGlyGCC, GlyCCC GlyTCC isodecoders, while expression changes in non-glycinergic tRNAs were minimal (4/152). Altogether, 1488/5820 proteins were sensitive to neuronal Nsun2-deficiency, in conjunction with GCC and CCC codon-specific defects in translational efficiencies and loss of Gly-rich proteins critical for glutamatergic neurotransmission, resulting in impaired synaptic signaling at PFC pyramidal neurons and impairments in contextual fear memory. These distortions in the neuronal translatome were associated with an adaptive, 2.46-fold up-regulation in PFC glycine levels with increased expression of multiple enzymes in the glycine biosynthetic pathway. These findings highlight the methylation sensitivity of glycinergic tRNAs in the adult PFC and link synaptic plasticity and complex behaviors to epitranscriptomic regulation of cognate tRNAs and the proteomic homeostasis associated with specific amino acids.

2021-07-01 | GSE165202 | GEO

Neuronal Nsun2 deficiency is associated with codon-specific epitranscriptomic dysregulation of Gly-tRNAs and corresponding proteomic shift impacting synaptic signaling and behavior

Project description:The role of transfer (t)RNA cytosine methyl-transferases as epitranscriptomic regulators of brain proteomes remains unexplored. We report that fear memory and antidepressant-like behaviors are highly sensitive to bi-directional changes in Nsun2 tRNA methyltransferase activity in prefrontal cortex (PFC) neurons. Nsun2-deficient mutant cortex showed a selective deficit in multiple glycine tRNAs, resulting in codon-specific shifts in translational efficiencies and a distorted proteomic landscape with deficits in glycine-rich neuronal proteins impacting synaptic signaling and behavior.

2021-07-02 | PXD023437 | Pride

NSun2-mediated cytosine-5 methylation in Vault non-coding RNA determines its processing into small RNAs [RNA-seq]

Project description:Autosomal-recessive loss of the NSUN2 gene has been recently identified as a causative link to intellectual disability disorders in humans. NSun2 is an RNA methyltransferase modifying cytosine-5 in transfer RNAs (tRNA). Whether NSun2 methylates additional RNA species is currently debated. Here, we adapted the individual-nucleotide resolution UV cross-linking and immunoprecipitation method (iCLIP) to identify NSun2-mediated methylation in RNA transcriptome. We confirm site-specific methylation in tRNA and identify messenger and non-coding RNAs as potential methylation targets for NSun2. Using RNA bisulfite sequencing we establish Vault non-coding RNAs as novel substrates for NSun2 and identified six cytosine-5 methylated sites. Furthermore, we show that loss of cytosine-5 methylation in Vault RNAs causes aberrant processing into argonaute-associating small RNA fragments (svRNA). Thus, impaired Vault non-coding RNA processing may be an important contributor to the etiology of NSUN2-deficieny human disorders. mRNA-seq in Embryonic kidney (HEK293) cells transfected with siRNA against Nsun2 vs control

2013-07-23 | E-GEOD-44384 | biostudies-arrayexpress

NSun2-mediated cytosine-5 methylation in Vault non-coding RNA determines its processing into small RNAs [iCLIP]

Project description:Autosomal-recessive loss of the NSUN2 gene has been recently identified as a causative link to intellectual disability disorders in humans. NSun2 is an RNA methyltransferase modifying cytosine-5 in transfer RNAs (tRNA). Whether NSun2 methylates additional RNA species is currently debated. Here, we adapted the individual-nucleotide resolution UV cross-linking and immunoprecipitation method (iCLIP) to identify NSun2-mediated methylation in RNA transcriptome. We confirm site-specific methylation in tRNA and identify messenger and non-coding RNAs as potential methylation targets for NSun2. Using RNA bisulfite sequencing we establish Vault non-coding RNAs as novel substrates for NSun2 and identified six cytosine-5 methylated sites. Furthermore, we show that loss of cytosine-5 methylation in Vault RNAs causes aberrant processing into argonaute-associating small RNA fragments (svRNA). Thus, impaired Vault non-coding RNA processing may be an important contributor to the etiology of NSUN2-deficieny human disorders. Identification of Nsun2 targets by miCLIP in Embryonic kidney (HEK293) cells

2013-07-23 | E-GEOD-44385 | biostudies-arrayexpress

tRNA gene identity acts as a determinant of gene positioning

2012-06-14 | GSE30103 | 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