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The role and mechanism of METTL16 in Alzheimer's disease

ABSTRACT: Mettl16 regulates SAM homeostasis by mediating m6A modification of MAT2A mRNA and participates in the pathogenesis of Alzheimer's disease.

ORGANISM(S): Mus Musculus

SUBMITTER: Huixian Cui

PROVIDER: PXD032022 | iProX | Thu Mar 03 00:00:00 GMT 2022

REPOSITORIES: iProX

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Knockdown of METTL16 disrupts learning and memory by reducing the stability of MAT2A mRNA.

Zhang Runjiao R Zhang Yizhou Y Guo Fangzhen F Huang Guannan G Zhao Yan Y Chen Bingyu B Wang Chang C Cui Chengran C Shi Yichun Y Li Sha S Cui Huixian H

Cell death discovery 20221028 1

N6-methyladenosine (m<sup>6</sup>A) is abundant in the mammalian brain and is considered to have a wide range of effects on learning and memory. Here, we found that the upregulated methyltransferase-like protein 16 (METTL16) in the hippocampal tissues of Morris water maze (MWM)-trained mice contributed to improved memory formation and hippocampal synaptic plasticity. Mechanismly, METTL16 promoted the expression of methionine adenosyltransferase 2A (MAT2A) by the m<sup>6</sup>A methylation of the ...[more]

PMID: 36307396

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TTP protects against acute liver failure by regulating CCL2 and CCL5 through m6A RNA methylation

Project description:Tristetraprolin (TTP), an important immunosuppressive protein regulating mRNA decay through recognizing the AU-rich elements (AREs) within the 3’UTRs of mRNAs, participates in the pathogenesis of liver diseases. However, whether TTP regulates mRNA stability through other mechanisms remains poorly understood. Here, we report that TTP is upregulated in acute liver failure (ALF), resulting in decreased mRNA stabilities of C-C Motif Chemokine Ligand 2 (CCL2) and C-C Motif Chemokine Ligand 5 (CCL5) through promoting N6-methyladenosine (m6A) mRNA methylation. Overexpression of TTP can markedly ameliorate hepatic injury in vivo. TTP regulates the mRNA stabilization of CCL2 and CCL5. Interestingly, increased m6A methylation in CCL2 and CCL5 mRNAs promotes TTP-mediated RNA destabilization. Moreover, induction of TTP upregulates expression levels of WT1 associated protein (WTAP), Methyltransferase like 14 (METTL14), and YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), which encode enzymes regulating m6A methylation, resulting in a global increase of m6A methylation and amelioration of live injury due to enhanced degradation of CCL2 and CCL5. These findings suggest a novel mechanism by which TTP modulates mRNA stabilities of CCL2 and CCL5 through m6A RNA methylation, which is involved in the pathogenesis of ALF.

2021-11-08 | GSE157581 | GEO

N6-methyl adenosine (m6A) recruits and repels proteins to regulate mRNA homeostasis

Project description:RNA modifications are integral to regulation of RNA metabolism. One such abundant mRNA modification is m6A, which impacts various aspects of RNA metabolism including splicing, transport and degradation. Current knowledge about proteins recruited to m6A to carry out these molecular processes is still limited. Here we describe a comprehensive and systematic mass spectrometry-based screening of m6A interactors in various cell types and species. Amongst the main findings, we identified G3BP1 as a protein, which is repelled by m6A and which positively regulates mRNA stability in an m6A regulated manner. Furthermore, we identified FMR1 as a novel, RNA sequence context dependent m6A reader, thus revealing a connection between an mRNA modification and an autism spectrum disorder. Collectively, our data represents a rich resource for the community and sheds further light on the complex interplay between m6A, m6A interactors and mRNA homeostasis.

2017-08-22 | PXD006498 | Pride

YTHDF2-m6A-NF-kB axis controls anti-tumor immunity through regulating intratumoral Treg survival and function

Project description:N6-methyladenosine (m6A) in messenger RNA (mRNA) regulates immune cells in homeostasis and in response to infection and inflammation. The function of YTHDF2 in the tumor microenvironment (TME) in these contexts has not been explored. We discovered that loss of Ythdf2 in regulatory T (Treg) cells can reduce tumor growth in mice while maintaining peripheral homeostasis. In the tumor microenvironment, Ythdf2-deficient Treg cells have impaired function and poor survival. The elevated tumor necrosis factor (TNF) signaling in the TME grants the location-specific function of YTHDF2, which participates in the feedback regulation of NF-kB signaling by accelerating the degradation of m6A-modified, NF-kB negative regulators, Nlrc3, Nfkbie, and Traf3. TME-specific regulation of Treg by YTHDF2 points to YTHDF2 as a target for anti-cancer immunotherapy, where intratumoral Treg cells can be targeted to enhance antitumor immune response, while avoiding Treg cells in the periphery to minimize undesired inflammations.

2023-06-07 | GSE230418 | GEO

YTHDF2-m6A-NF-kB axis controls anti-tumor immunity through regulating intratumoral Treg survival and function [RNA-seq]

2023-06-07 | GSE216959 | GEO

YTHDF2-m6A-NF-kB axis controls anti-tumor immunity through regulating intratumoral Treg survival and function [RIP-seq]

2023-06-07 | GSE216958 | GEO

MYC Promotes Cancer Progression by Modulating m6A Modification to Suppress Target Gene Translation

Project description:N6-Methyladenosine (m6A) is the most prevalent internal modification in mammalian mRNAs, and participates in various fundamental bioprocesses as well as cancer. Here we immunoprecipitated m6A methylated poly (A+) RNAs (MeRIP) and then sequenced and profiled mRNA m6A methylation in P493-6 cells.

2020-12-18 | GSE150892 | GEO

Puri2010 - Mathematical Modeling for the Pathogenesis of Alzheimer's Disease

Project description:Puri2010 - Mathematical Modeling for the Pathogenesis of Alzheimer's Disease Puri2010 - Mathematical Modeling for the Pathogenesis of Alzheimer's Disease Encoded non-curated model. Issues: - Confusing replacement of α16 when t = 3 years - Confusing 4th rate equation This model is described in the article: Mathematical modeling for the pathogenesis of Alzheimer's disease. Puri IK, Li L. PLoS ONE 2010; 5(12): e15176 Abstract: Despite extensive research, the pathogenesis of neurodegenerative Alzheimer's disease (AD) still eludes our comprehension. This is largely due to complex and dynamic cross-talks that occur among multiple cell types throughout the aging process. We present a mathematical model that helps define critical components of AD pathogenesis based on differential rate equations that represent the known cross-talks involving microglia, astroglia, neurons, and amyloid-? (A?). We demonstrate that the inflammatory activation of microglia serves as a key node for progressive neurodegeneration. Our analysis reveals that targeting microglia may hold potential promise in the prevention and treatment of AD. This model is hosted on BioModels Database and identified by: MODEL1409240001. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

2015-04-15 | MODEL1409240001 | BioModels

Profiling of N6-Adenosine (m6A) Methylation in Arabidopsis thaliana wild-type and fip37-4 LEC1:FIP37

Project description:N6-methyladenosine (m6A) represents the most prevalent internal modification on messenger RNA, and requires a multicomponent m6A methyltransferase complex in mammals. How their plant counterparts determine the global m6A modification landscape and its molecular link to plant development remain elusive. Here we show that FKBP12 INTERACTING PROTEIN 37 KD (FIP37) is a core component of the m6A methyltransferase complex, which underlies control of shoot stem cell fate in Arabidopsis. The mutants lacking FIP37 exhibit massive overproliferation of shoot meristems and a transcriptome-wide loss of m6A RNA modifications. We further demonstrate that FIP37 mediates m6A RNA modification on key shoot meristem genes inversely correlated with their mRNA stability, thus confining their transcript levels to prevent shoot meristem overproliferation. Our results suggest an indispensable role of FIP37 in mediating m6A mRNA modification, which is required for maintaining the shoot meristem as a renewable source for continuously producing all aerial organs in plants. m6A-seq in Arabidopsis thaliana (Col-0) wild-type and fip37-4 LEC1:FIP37, two replicates for each sample

2016-07-25 | E-GEOD-75506 | biostudies-arrayexpress

Differential Methylation of CircRNA m6A in the APP/PS1 Alzheimer's Disease Mouse Model [cirRNA-seq]

Project description:Alzheimer's disease (AD) is a chronic neurological disease which characterized as memory loss and progressive cognitive impairment. The characteristic of AD pathologies include extracellular senile plaques formed by β-amyloid protein deposition, neurofifibrillary tangles formed byhyper-phosphorylation of tau protein, and neuronal loss caused by glial cell proliferation. However, the pathogenesis of AD is still unclear. Resent research have shown that the dysregulation of RNA methylation is related to many biological processes, including neurodevelopment and neurodegenerative diseases. N6-methyladenosine (m6A) is the mainly modification in eukaryotic RNA, and it may be associated with the pathophysiology of AD. Circular RNA (circRNA) is a new type of evolutionarily conserved non-coding RNA without 5’cap and 3’polyadenylic acid tail. Recent studies suggested that circRNA may involved in the pathogenesis of AD. m6A RNA methylation is also found in circRNAs. In this study, we performed high-throughput sequencing on the degree of circRNA m6A methylation in APP/PS1 AD and C57BL/6 mice. The results suggest that circRNA m6A methylation degree in AD mice is different compared to the control group. In addition, using gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis to predict related pathways, the results showed that the genes with different circRNA m6A methylation in AD mice is associated with axon guidance, long-term potentiation, glutama tergic synapse, cholinergic synapse, gabaergic synapse and long-term depression. The MeRIP-qPCR results showed that among the 8 selected circRNA m6A genes, there are 5 genes with increased methylation and others with decreased methylation. In summary, the results of this study indicate that circRNA m6A methylation may related to the pathogenesis of AD.

2022-11-03 | GSE216901 | GEO

the Arraystar Human m6A-mRNA&lncRNA Epitranscriptomic microarray analysis in the neutrophils of ischemic stroke patients and healthy controls

Project description:The high incidence, mortality, and disability rate of ischemic stroke impose huge economic burdens on patients and social health care systems.N6-methyladenosine (m6A) is one of the most extensive RNA methylation modifications in eukaryotes and participates in the pathogenesis of numerous diseases including ischemic stroke. Peripheral blood neutrophils are forerunners after ischemic brain injury and exert crucial functions.However, the underlying mechanisms of neutrophils in ischemic stroke need to be further clarified. This study aims to explore the transcriptional profiles of m6A modification in neutrophils of patients with ischemic stroke. The Arraystar Human m6A-mRNA&lncRNA Epitranscriptomic microarray analysis was performed on the peripheral blood neutrophils of 3 patients with ischemic stroke and 3 healthy controls, providing the clinical significance of m6A modification on ischemic stroke.

2023-07-08 | GSE236381 | GEO

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