Dynamic N6-methyladenosine Epitranscriptomic Landscape in Lung Adenocarcinoma
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ABSTRACT:
PROVIDER: EGAS00001005524 | EGA |
REPOSITORIES: EGA
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2022-02-18 | GSE189874 | GEO
Project description:Chemical modification of RNAs is important for post-transcriptional gene regulation. The METTL3-METTL14 complex generates most N6-methyladenosine (m6A) modifications in mRNAs, and dysregulated methyltransferase expression has been linked to numerous cancers. Here we show that m6A modification location, rather than the overall modification level, can impact oncogenesis. A gain-of-function missense mutation found in cancer patients, METTL14R298P, promotes malignant cell growth in culture and in transgenic mice. The mutant methyltransferase preferentially modifies noncanonical sites and transforms gene expression without increasing global m6A levels in mRNAs. The altered substrate specificity is intrinsic to METTL3-METTL14, helping us to propose a structural model for how the METTL3-METTL14 complex detects RNA sequences. Together, our work highlights that m6A location is important for function and that noncanonical methylation sites may impact aberrant gene expression and oncogenesis.
2024-12-21 | PXD039447 | Pride
Project description:In this study, we aimed to systematically profile global RNA N6-methyladenosine (m6A) modification patterns in a mouse model of diabetic cardiomyopathy (DCM). Patterns of m6A in DCM and normal hearts were analyzed via m6A-specific methylated RNA immunoprecipitation followed by high-throughput sequencing (MeRIP-seq) and RNA sequencing (RNA-seq). A total of 973 m6A peaks were detected in DCM samples and 296 differentially methylated sites were selected for further study, including 106 hypermethylated and 190 hypomethylated m6A sites (fold change (FC) > 2, p < 0.05). Gene ontology and KEGG Pathway analyses indicated that unique m6A-modified transcripts in DCM were closely linked to cardiac fibrosis, myocardial hypertrophy, and myocardial energy metabolism. Overall, m6A modification patterns were altered in DCM, and modification of epitranscriptomic processes, such as m6A, is a potentially interesting therapeutic approach.
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Project description:Aim: To systematically classify the profile of the RNA m6A modification landscape of neonatal heart regeneration. Materials and Methods: Cardiomyocyte proliferation markers were detected via immunostaining. The expression of m6A modification regulators was detected using quantitative real-time PCR (qPCR) and Western blotting. Genome-wide profiling of m6A-modified transcripts was conducted with m6A-modified RNA immunoprecipitation sequencing (m6A-RIP-seq) and RNA sequencing (RNA-seq). The Gene Expression Omnibus database (GEO) dataset was used to verify the hub genes. Results: METTL3 and the level of m6A modification in total RNA were lower in P7 rat hearts than in P0 ones. In all, 1637 m6A peaks were differentially expressed using m6A-RIP-seq, with 84 upregulated and 1553 downregulated. Furthermore, conjoint analyses of m6A-RIP-seq, RNA-seq, and GEO data generated eight potential hub genes with differentially expressed hypermethylated or hypomethylated m6A levels. Conclusion: Our data show novel information on m6A modification changes in cardiac regeneration. The modifications made possible by directly modulating m6A may attract future study of cardiac regeneration.
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Project description:N6-methyladenosine (m6A), the most abundant mRNA modification, was shown to alter the life cycles of diverse DNA and RNA viruses. These effects were proposed to be mediated in a virus-specific manner, through dysregulated methylation of viral RNA. We use RNA-seq to systematically follow differences in gene expression in cells depleted of m6A machinery, compared to control cells, following human cytomegalovirus (HCMV) infection. We show that following viral infection or stimulation of cells with an inactivated virus, depletion of the m6A 'writer' protein METTL3 or 'reader' protein YTHDF2 leads to a dramatic increase in the induction of hundreds of interferon-stimulated genes (ISGs), which constitutes the first line of antiviral defense. Consequently, propagation of different viruses is markedly suppressed in an interferon (IFN)-signaling dependent manner. Furthermore, we used m6A-immunoprecipitation, followed by RNA-seq, to map m6A sites on human and HCMV transcripts, and found that the mRNA of IFNβ, the central cytokine that drives the type I IFN response, is m6A modified, and is stabilized upon repression of METTL3 and YTHDF2.
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Project description:N6-methyladenosine (m6A) is the most ubiquitous mRNA base modification, but little is known about its precise location, temporal dynamics, and regulation. Here, we generated genomic maps of m6A sites in meiotic yeast transcripts at nearly single-nucleotide resolution, identifying 1,308 putatively methylated sites within 1,183 transcripts. We validated 8/8 methylation sites in different genes with direct genetic analysis, demonstrated that methylated sites are significantly conserved in a related species, and built a model that predicts methylated sites directly from sequence. Sites vary in their methylation profiles along a dense meiotic time-course, and are regulated both locally, via predictable methylatability of each site, and globally, through the core meiotic circuitry. The methyltransferase complex components localize to the yeast nucleolus, and this localization is essential for mRNA methylation. Our data illuminates a conserved, dynamically regulated methylation program in yeast meiosis, and provides an important resource for studying the function of this epitranscriptomic modification. Examination of m6A methylation under various conditions
2013-11-22 | E-GEOD-51583 | biostudies-arrayexpress
Project description:Context: Long non-coding RNAs (lncRNAs) regulate pathological processes, yet their potential roles in papillary thyroid carcinoma (PTC) are poorly understood. Objective: To profile transcriptionally dysregulated lncRNAs in PTC and identify lncRNAs associated with clinicopathological characteristics. We performed RNA sequencing of 12 paired PTC tumors and matched noncancerous tissues and correlated the expression of lncRNAs with clinical parameters.
2016-08-03 | E-GEOD-83520 | biostudies-arrayexpress
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2018-01-31 | GSE100546 | GEO