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RNA transcriptome analyses in Nup93R388W-knock in (KI) mice (strain: 129S1/SvlmJ)

ABSTRACT: To investigate the role of m6A in RNA export, we performed transcriptome profiling by high throughput sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE310336 | GEO | 2025/12/30

REPOSITORIES: GEO

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N6-methyladenosine RNA methylome analyses in podocytes of Nup93R388W-knock in (KI) mice (strain: 129S1/SvlmJ)

Project description:To identify N6-methyladenosine RNA methylome, we performed MeRIP-seq using murine podocytes isolated from Nup93R388W-knock in (KI) mice

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RNA transcriptome analyses in Nup93R388W-knock in (KI) mice (strain: 129S1/SvlmJ)

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RNA transcriptome analyses in shMETTL3 and shNUP93 in LNCaP, Hela and podocyte cells

Project description:To investigate the role of m6A in RNA export, we performed transcriptome profiling by high throughput sequencing.

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N6-methyladenosine RNA methylome analyses in podocytes of Nup93R388W-knock in (KI) mice (strain: 129S1/SvlmJ)

Project description:N6-methyladenosine RNA methylome analyses in podocytes of Nup93R388W-knock in (KI) mice (strain: 129S1/SvlmJ)

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N6-adenosine methylation enhances nuclear mRNA export through METTL3 and NUP93

Project description:Nuclear export of messenger RNAs (mRNAs) through nuclear pore complexes (NPCs) is a critical step in gene expression. Although N6-adenosine methylation (m6A) has been implicated in this process, the underlying mechanism remains obscure. Here, using single-molecule imaging, we demonstrate that m6A markedly accelerates nuclear export of messenger ribonucleoproteins (mRNPs) by increasing export efficiency and shortening export time through NPCs. We further show that the m6A methyltransferase METTL3 localizes at NPCs and functionally associates with the nucleoporin NUP93 to promote efficient export of m6A-modified mRNPs. Disruption of this functional association between METTL3 and NUP93 substantially impairs overall mRNP export efficiency. Notably, a steroid-resistant nephrotic syndrome (SRNS)-associated NUP93 variant (c.1162C>T, p.Arg388Trp) fails to associate with METTL3, resulting in defective nuclear export of key methylated mRNAs required for kidney function. Together, our findings define an m6A-METTL3-NUP93 regulatory axis for nuclear mRNA export with broad implications for human disease.

2025-12-23 | MSV000100322 | MassIVE

Phospho-antibody microarray analyses for islets of control and Mettl14 knock-out mice

Project description:β-cell specific Mettl14 knock-out mice display reduced N6-methyladenosine (m6A) levels and recapitulate human Type II diabetes (T2D) islet phenotype with early diabetes onset and mortality secondary to decreased β-cell proliferation and insulin degranulation. To gain insights into the role of m6A in regulating the IGF1/insulin -> AKT - > PDX1 pathway and to dissect the signaling networks modulating AKT phosphorylation, we subjected freshly isolated islets from control and Mettl14 knock-out mice to phospho-antibody microarrays.

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RNA transcriptome analyses in shcontrol, shMETTL3, shMETTL3-resistant METTL3 wildtype and catalytically dead mutant LNCaP cells.

Project description:To investigate the role of METTL3-mediated m6A modification, we performed transcriptome profiling by high throughput sequencing.

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Behavioral and Transcriptome Profiling of Heterozygous Rab10 Knock-Out Mice.

Project description:A central question in the field of aging research is to identify the cellular and molecular basis of neuroresilience. One potential candidate is the small GTPase, Rab10. Here, we used Rab10+/- mice to investigate the molecular mechanisms underlying Rab10-mediated neuroresilience. Brain expression analysis of 880 genes involved in neurodegeneration showed that Rab10+/- mice have increased activation of pathways associated with neuronal metabolism, structural integrity, neurotransmission, and neuroplasticity compared with their Rab10+/+ littermates. Lower activation was observed for pathways involved in neuroinflammation and aging. We identified and validated several differentially expressed genes (DEGs), including Stx2, Stx1b, Vegfa, and Lrrc25 (downregulated) and Prkaa2, Syt4, and Grin2d (upregulated). Behavioral testing showed that Rab10+/- mice perform better in a hippocampal-dependent spatial task (object in place test), while their performance in a classical conditioning task (trace eyeblink classical conditioning, TECC) was significantly impaired. Therefore, our findings indicate that Rab10 differentially controls the brain circuitry of hippocampal-dependent spatial memory and higher-order behavior that requires intact cortex-hippocampal circuitry. Transcriptome and biochemical characterization of these mice suggest that glutamate ionotropic receptor NMDA type subunit 2D (GRIN2D or GluN2D) is affected by Rab10 signaling. Further work is needed to evaluate whether GRIN2D mediates the behavioral phenotypes of the Rab10+/- mice. We conclude that Rab10+/- mice described here can be a valuable tool to study the mechanisms of resilience in Alzheimer's disease (AD) model mice and to identify novel therapeutical targets to prevent cognitive decline associated with normal and pathologic aging.

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Sex-specific associations between AD genotype and the microbiome of human amyloid beta knock-in (hAβ-KI) mice.

Project description:IntroductionEmerging evidence links changes in the gut microbiome to late-onset Alzheimer's disease (LOAD), necessitating examination of AD mouse models with consideration of the microbiome.MethodsWe used shotgun metagenomics and untargeted metabolomics to study the human amyloid beta knock-in (hAβ-KI) murine model for LOAD compared to both wild-type (WT) mice and a model for early-onset AD (3xTg-AD).ResultsEighteen-month female (but not male) hAβ-KI microbiomes were distinct from WT microbiomes, with AD genotype accounting for 18% of the variance by permutational multivariate analysis of variance (PERMANOVA). Metabolomic diversity differences were observed in females, however no individual metabolites were differentially abundant. hAβ-KI mice microbiomes were distinguishable from 3xTg-AD animals (81% accuracy by random forest modeling), with separation primarily driven by Romboutsia ilealis and Turicibacter species. Microbiomes were highly cage specific, with cage assignment accounting for more than 40% of the PERMANOVA variance between the groups.DiscussionThese findings highlight a sex-dependent variation in the microbiomes of hAβ-KI mice and underscore the importance of considering the microbiome when designing studies that use murine models for AD.HighlightsMicrobial diversity and the abundance of several species differed in human amyloid beta knock-in (hAβ-KI) females but not males. Correlations to Alzheimer's disease (AD) genotype were stronger for the microbiome than the metabolome. Microbiomes from hAβ-KI mice were distinct from 3xTg-AD mice. Cage effects accounted for most of the variance in the microbiome and metabolome.

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The m 6 A-methylase complex recruits TREX and regulates mRNA export.

Project description:N6-methyladenosine (m6A) is the most abundant internal modification of eukaryotic mRNA. This modification has previously been shown to alter the export kinetics for mRNAs though the molecular details surrounding this phenomenon remain poorly understood. Here we show that the m6A complex (WTAP, KIAA1429, METTL3/14) drives recruitment of the TREX mRNA export complex onto m6A modified mRNAs and this process is essential for the efficient export of certain mRNAs. Depletion of the core m6A complex leads to loss of TREX from mRNAs which undergo the m6A modification. We show that TREX stimulates recruitment of the m6A reader protein YTHDC1 to the mRNP and the m6A complex influences the interaction of TREX with YTHDC1. We suggest that m6A acts as a surrogate for other TREX recruitment mechanisms such as splicing and 5’ capping, in long internal and final exons which may otherwise be devoid of this essential complex for mRNA export.

2018-10-03 | GSE111878 | GEO

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