Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency [ChIP-seq]

ABSTRACT: Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency [ChIP-seq]

PROVIDER: PRJNA869466 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21047020.fastq.gz	Fastqsanger.gz
	SRR21047021.fastq.gz	Fastqsanger.gz
	SRR21047022.fastq.gz	Fastqsanger.gz
	SRR21047023.fastq.gz	Fastqsanger.gz
	SRR21047024.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency [iCLIP]

Project description:Post-transcriptional modifications of mRNA have emerged as novel regulators of gene expression. Pseudouridylation is the most abundant and widespread type of RNA modification in living organisms; however, the biological role of pseudouridine in mRNAs remains poorly understood. Here, we show that the pseudouridine synthase dyskerin associates with RNA polymerase II and is enriched at RNA polymerase II-transcribed genes genome-wide. As part of the H/ACA complex, dyskerin binds to thousands of mRNAs and is responsible for their pseudouridylation, an action that occurs in chromatin and does not appear to require a fully complementary guide RNA. In cells lacking dyskerin, pseudouridylation of mRNAs is reduced, while at the same time, de novo protein production is enhanced, indicating that pseudouridylation of mRNAs by dyskerin interferes with translation. Accordingly, pseudouridylation of an mRNA by dyskerin in vitro results in reduced translation of that mRNA. Moreover, in patients with dyskeratosis congenita caused by inherited mutations in the DKC1 gene, binding between mutated dyskerin and mRNAs is altered and pseudouridylation of mRNAs severely reduced. Our findings reveal a new critical function of the H/ACA complex in directing translation control with important implications for development and disease.

2023-06-26 | GSE211201 | GEO

Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency [RNA-seq]

2023-06-26 | GSE211200 | GEO

Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency [ChIP-seq]

2023-06-26 | GSE211199 | GEO

Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency.

Project description:Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency.

| PRJNA869465 | ENA

Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency [iCLIP]

Project description:Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency [iCLIP]

| PRJNA869468 | ENA

Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency [RNA-seq]

Project description:Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency [RNA-seq]

| PRJNA869467 | ENA

Pseudouridylation in Naf1+/- mice

Project description:Pseudo-seq was used to measure differences in the extent of pseudouridine (Î¨) modification in rRNA from mice haploinsufficient for the H/ACA biogenesis factor Naf1 compared to wild- type. We measured telomerase RNA levels as well as a sample of box H/ACA RNAs and found they were all decreased in Naf1+/- mice. Nevertheless, Naf1+/- mice had minimally decreased levels of pseudouridylation at the rRNA sites queried. This was not associated with any phenotypic abnormalities in vivo in these mice which we examined for hematopoeitic, liver, testes and brain defects. CMC treatment of RNA followed by next generation sequencing was used to measure the extent of pseudouridylation at mapped mouse rRNA Î¨ sites.

2016-08-07 | E-GEOD-78063 | biostudies-arrayexpress

Co-transcriptional pseudouridylation of mRNAs by the H/ACA complex controls translational efficiency.

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-26 | GSE211202 | GEO

Impact of G-content on Arabidopsis AtPAB binding and their role in enhancing translational efficiency

Project description:Polyadenylation plays a key role in producing mature mRNAs in eukaryotes. It is widely believed that the poly(A)-binding proteins (PABs) uniformly bind to poly(A)-tailed mRNAs, regulating their stability and translational efficiency. Here, we characterized the RNA-binding landscape of three broadly expressed PABs in Arabidopsis thaliana. We observed substantial variation in the AtPAB-binding efficiency among mRNAs, which can be partly explained by the guanosine (G) content of poly(A) tails. AtPAB-binding efficiency of a gene was positively associated with translational efficiency rather than mRNA stability. Consistently, genes with stronger AtPAB binding exhibited a greater reduction in translational efficiency when AtPAB is depleted. Our study provides a new mechanism that translational efficiency of a gene can be regulated through G-content-dependent PAB binding, paving the way for a better understanding of poly(A) tail-associated regulation of gene expression.

2019-08-14 | GSE110342 | GEO

Pseudouridylation in Naf1+/- mice

Project description:Pseudo-seq was used to measure differences in the extent of pseudouridine (Ψ) modification in rRNA from mice haploinsufficient for the H/ACA biogenesis factor Naf1 compared to wild- type. We measured telomerase RNA levels as well as a sample of box H/ACA RNAs and found they were all decreased in Naf1+/- mice. Nevertheless, Naf1+/- mice had minimally decreased levels of pseudouridylation at the rRNA sites queried. This was not associated with any phenotypic abnormalities in vivo in these mice which we examined for hematopoeitic, liver, testes and brain defects.

2016-08-07 | GSE78063 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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