Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

59 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Obesity-associated Fto gene regulates activity of the dopaminergic midbrain circuitry [FTO KO]

ABSTRACT: Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission. Profiling of m6A in midbrain and striatum from FTO knockout mice

ORGANISM(S): Mus musculus

SUBMITTER: Christopher Mason

PROVIDER: E-GEOD-47216 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

The Obesity-associated Fto gene regulates activity of the dopaminergic midbrain circuitry [WT]

Project description:Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission. Profiling of m6A in midbrain and striatum from wild type mice

2013-06-15 | E-GEOD-47215 | biostudies-arrayexpress

The Obesity-associated Fto gene regulates activity of the dopaminergic midbrain circuitry [FTO KO]

2013-06-15 | GSE47216 | GEO

The Obesity-associated Fto gene regulates activity of the dopaminergic midbrain circuitry [WT]

2013-06-15 | GSE47215 | GEO

Comprehensive Analysis of mRNA Methylation Reveals Enrichment in 3' UTRs and Near Stop Codons (OLD)

Project description:Here, we use a novel technique for locating regions of N6-adenosine methylation (m6A) throughout the transcriptome and present a profile of m6A sites in the mouse brain. Our use of methylated RNA immunoprecipitation combined with RNA-seq (MeRIP-Seq) identifies thousands of RNAs which contain m6A sites. In addition, we find that regions of m6A formation are particularly enriched near stop codons, which might provide clues into the potential funciton of this highly prevalent RNA modificaiton. Examination of m6A sites in murine brain RNA and human embryonic kidney cells.

2012-12-31 | E-GEOD-34734 | biostudies-arrayexpress

Adenosine methylation is widespread throughout the transcriptome and prominent within 3' UTRs

2012-05-16 | E-GEOD-29714 | biostudies-arrayexpress

m6a peak analysis in normal, FTO deficient and five stages of adipogenesis (D-2/0/2/5/10) in Mouse embryo fibroblast 3T3-L1 pre-adipocytes

Project description:Total RNA was extracted using TRI® Reagent (Sigma). cDNA was synthesized by RevertAid™ First Strand cDNA Synthesis Kit with Oligo dT primers (K1622, Fermentas) following manufacturer’s recommendations. PCR reactions were carried out on a DNAEngine® Thermal Cycler (PTC-0200G, Bio-Rad) in 25 μl reaction volume containing 1 μl cDNA, 200 nM primer pairs and components of TaKaRa Taq™ kit (R001A, Takara). All samples were analyzed in triplicate RT-qPCR.mRNAs were extracted using biotinylated poly(dT) oligo, followed by further removing of contaminated rRNA using RiboMinus Transcriptome Isolation Kit (K1550-02, Invitrogen). Then mRNAs were fragmented into 100-200nt length and subjected to immunoprecipitation with m6A specific antibody.The libraries were sequenced using HiSeq2000 (Illumina) in single-read mode, creating reads with a length of 101 bp. Sequencing chemistry v2 (Illumina) was used and samples were multiplexed in two samples per lane. discovery of the binding motif of m6a in normal, FTO deficient and five stages of adipogensis (D-2/0/2/5/10) in Mouse embryo ﬁbroblast 3T3-L1 pre-adipocytes

2015-03-09 | E-GEOD-53244 | biostudies-arrayexpress

Activin/Nodal-dependent N6-methyladenosine (m6A) deposition in human pluripotent stem cells

Project description:This experiment was designed to probe the function of Activin/Nodal signalling in the deposition of m6A in human pluripotent stem cells (hPSCs). hPSCs were cultured in presence of Activin or subjected to short-term inhibition of Activin/Nodal signalling for 2h using the receptor antagonist SB-431542 (IP). The global abundance of m6A was then measured by nuclear-enriched methylated RNA immunoprecipitation followed by deep sequencing (NeMeRIP-seq). Pre-NeMeRIP input RNA was used as control to normalise for the changes in gene expression in the two conditions.

2017-12-26 | E-MTAB-5229 | biostudies-arrayexpress

The interacted proteins of ALKBH5 and FTO identified by IP-mass

Project description:Since m6A demethylases (FTO and ALKBH5) have been reported to be involved in pre-mRNA splicing regulation, we hypothesized that dynamic m6A distribution during mRNA maturation might involve removal of m6A in internal exons by FTO or ALKBH5 accompanied by splicing factors. To explore this we performed pull-down assays coupled with protein mass spectrometry.

2022-12-09 | PXD038705 | Pride

The Obesity-associated Fto gene regulates activity of the dopaminergic midbrain circuitry

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-15 | E-GEOD-47217 | biostudies-arrayexpress

Quantitative Proteomics of Mouse Liver (FTO-KO,WT) in response to DEN injection

Project description:Single nucleotide polymorphisms in the FTO gene encoding a m6A demthylase are associated with obesity and cancer development. However, the functional role of FTO in the developemnt of progression of hepatocellular carcinoma (HCC) as a proteotypic obesity-associated cancer remains unclear. Here, we have generated mice with hepatic FTO deficiency (FTOL-KO) and subjected them to DEN induced HCC-development. FTOL-KO mice exhibit increased HCC burden. While control mice exhibit a dynamic regulation of FTO upon induction of liver damage, this response is abrogated in mice lacking FTO. Proteomic analyses revealed that liver damage-induced increases in FTO expression promotes m6A-demethylation of CUL4A reducing its protein expression. Functionally, knockdown of CUL4A restores the increased hepatocyte proliferation observed upon loss of FTO. Collectively, our study reveals a protective role for FTO-dependent dynamic m6A mRNA demethylation of CUL4A in the initiation of HCC development.

2020-11-03 | PXD018223 | Pride

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