Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mettl5 mediated 18S rRNA N6-methyladenosine (m6A) modification controls neural development and the learning and memory function

ABSTRACT: Mettl5 mediated 18S rRNA N6-methyladenosine (m6A) modification controls neural development and the learning and memory function

PROVIDER: PRJNA641584 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12081230_1.fastq.gz	Fastqsanger.gz
	SRR12081230_2.fastq.gz	Fastqsanger.gz
	SRR12081231_1.fastq.gz	Fastqsanger.gz
	SRR12081231_2.fastq.gz	Fastqsanger.gz
	SRR12081232_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 37

Similar Datasets

METTL5, an 18S rRNA-specific m6A methyltransferase, regulates the Integrated Stress Response [eCLIP]

Project description:RNA N6-methyladenosine (m6A) modification is present in different RNA molecules, including protein-coding mRNAs and non-coding RNAs such as ribosomal RNAs (rRNAs).Here, we report that mammalian METTL5, a member of a highly conserved methyltransferase family, specifically methylates adenosine 1832 (A1832) in the 18S rRNA in vivo and in vitro.

2020-09-17 | GSE138123 | GEO

Function and Mechanism of METTL5-mediated 18S rRNA m6A1832 modification in hepatocellular carcinoma

Project description:Tumor recurrence is main pattern of treatment failure for early-stage hepatocellular carcinoma (HCC). However, the molecular mechanisms underlying disease recurrence remain poorly understood. Here, we showed that 18S rRNA N6-methyladenosine (m6A1832) modification and its methyltransferase complex METTL5/TRMT112 were upregulated in HCC and correlated with poor prognosis. Loss-of-function and gain-of-function assays demonstrated that METTL5/TRMT112 mediated 18S rRNA m6A1832 modification promotes HCC tumorigenesis in vitro and in vivo. Mechanistically, 18S rRNA m6A1832 modification selectively regulated the translation of mRNAs with long 5’UTR and short 3’UTR through affecting the assembly of 80S subunit at translation initiation and its dissociation at translation termination which was executed by weakening the interaction of ABCE1 with eRF1 and eRF3. Moreover, METTL5-mediated 18S rRNA m6A1832 modification regulated β-oxidation of long-chain fatty acid through ACSL4 to promote HCC progression. Our work uncovered a novel layer of mRNA translation regulation mechanism at ribosome 80S subunit assembly and dissociation step mediated by 18S rRNA m6A1832 modification and revealed a new crosslink between RNA epigenetic modification and fatty acid metabolism in HCC.

2021-06-01 | GSE175827 | GEO

18S rRNA N6-methyladenosine (m6A) modification promotes tumorigenesis and chemoresistance via gain-of-function mutant p53 in nasopharyngeal carcinoma

Project description:Mis-regulated mRNA translation and hyperactivation of ribosome biogenesis are the two main hallmarks of cancer cells, whereas their intrinsic links and molecular mechanisms remain poorly understood. Our current study revealed that METTL5 and its mediated 18S rRNA N6-methyladenosine modification at 1832 position (m6A1832) are elevated in nasopharyngeal carcinoma (NPC) and correlated with disease progression. Gain-of-function and loss-of-function assays showed that METTL5 mediated 18S rRNA m6A1832 modification promotes NPC cells proliferation and metastasis in vitro and in vivo. Mechanistically, loss of 18S rRNA m6A1832 modification impairs the assembly of 80S ribosome and therefore affecting global mRNA translation. Furthermore, polyribosome-bound mRNA sequencing (Polyribosome-RNA-seq), ribosome profiling sequencing (Ribo-seq) and whole exome sequencing (WES) data identified a METTL5/HSF4b/HSP90B1/mutant p53 (mutp53) axis which contributed to NPC tumorigenesis and chemoresistance. Our findings uncovered a novel mechanism underlying rRNA epigenetic modification in regulating mRNA translation and mutp53 pathway in cancer.

2024-10-24 | GSE186485 | GEO

The human 18S rRNA m6A methyltransferase METTL5 is stabilized by TRMT112

Project description:N6-methyladenosine (m6A) has recently been found abundantly on messenger RNA and shown to regulate most steps of mRNA metabolism. Several important m6A methyltransferases have been described functionally and structurally, but the enzymes responsible for installing one m6A residue on each subunit of human ribosomes at functionally important sites have eluded identification for over 30 years. Here we identify METTL5 as the enzyme responsible for 18S rRNA m6A modification and confirm ZCCHC4 as the 28S rRNA modification enzyme. We show that METTL5 must form a heterodimeric complex with TRMT112, a known methyltransferase activator, to gain metabolic stability in cells. We provide the first atomic resolution structure of METTL5-TRMT112, supporting that its RNA binding mode differs distinctly from that of other m6A RNA methyltransferases. On the basis of similarities with a DNA methyltransferase, we propose that METTL5-TRMT112 acts by extruding the adenosine to be modified from a double-stranded nucleic acid.

2019-07-15 | GSE128699 | GEO

Methyltransferase METTL5 interactome

Project description:Cellular RNAs are covalently modified and these modifications can impact on all biological processes and hence are implicated in different types of diseases. Amongst RNA modifications, N6-methyladenosine (m6A) is one of the most widespread and has been found on messenger (mRNA), ribosomal (rRNA), non-coding and spliceosomal RNAs. We undertook a systematic screen to uncover new RNA-methyltransferases. We demonstrate that the methyltransferase-like 5 protein (METTL5) is an 18S rRNA specific methyltransferase and interacts specifically with Trmt122.

2020-09-09 | PXD015582 | Pride

Mapping N6-methyladenosine (m6A) peaks in wild-type and METTL5 knockout (KO) HeLa cells

Project description:We report the application of MeRIP-seq to map m6A peaks in wild type and METTL5 KO HeLa cells to investigate targets of the m6A methyltransferase METTL5.

2021-05-19 | GSE174420 | GEO

Mapping N6-methyladenosine (m6A) peaks in wild-type and METTL5 knockout (KO) HeLa cells

Project description:Mapping N6-methyladenosine (m6A) peaks in wild-type and METTL5 knockout (KO) HeLa cells

| PRJNA729867 | ENA

N6-methyladenosine (m6A) methylated RNA immunoprecipatation and sequencing in wildtype and Mettl5-/- embryonic stem cells.

Project description:N6-methyladenosine (m6A) methylated RNA immunoprecipatation and sequencing in wildtype and Mettl5-/- embryonic stem cells.

| PRJNA641588 | ENA

N6-Methyladenosine methylation profile in rat H9C2 cardiomyocytes under the hypoxic stress

Project description:Hypoxia as a crucial pathogenesis factor usually results in huge harmful effects on cardiac injury and dysfunction. In our previous study (PMID: 33294289), We observe a series of differential expressed genes between transcription and translation, which may be attributed to the hypoxia-specific binding affinity of Nuclear cap-binding subunit 3 (NCBP3) at 5’ un-translation region of target genes. But the underlying molecular mechanism of NCBP3 for gene translation modulation remains unclear. Here, we conducted RIP-seq of N6-Methyladenosine methylation in H9C2 cells with the conditions of normoxic, hypoxic and with additional NCBP3 knockdown.

2021-06-30 | E-MTAB-10682 | biostudies-arrayexpress

N6-methyladenosine Modulates Messenger RNA Translation Efficiency

Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down

2015-06-09 | E-GEOD-63591 | biostudies-arrayexpress

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