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Genomic N6-methyladenosine promotes expression of genes important for chromosome maintenance in bacteria

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Bacillus subtilis PY79 Bacillus subtilis

PROVIDER: GSE130695 | GEO | 2019/05/04

REPOSITORIES: GEO

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Genomic N6-methyladenosine promotes expression of genes important for chromosome maintenance in bacteria [pacbio_DnmA2]

Project description:We used Pacific Biosciences Single Molecule Real-Time sequencing platform to identify m6A modifications and putative methyltransferases in Bacillus subtilis

2019-05-04 | GSE130694 | GEO

Genomic N6-methyladenosine promotes expression of genes important for chromosome maintenance in bacteria [pacbio_DnmA]

Project description:We used Pacific Biosciences Single Molecule Real-Time sequencing platform to identify m6A modifications and putative methyltransferases in Bacillus subtilis

2019-05-04 | GSE130693 | GEO

Genomic N6-methyladenosine promotes expression of genes important for chromosome maintenance in bacteria

Project description:Genomic N6-methyladenosine promotes expression of genes important for chromosome maintenance in bacteria

| PRJNA540992 | ENA

Genomic N6-methyladenosine promotes expression of genes important for chromosome maintenance in bacteria [pacbio_DnmA]

Project description:Genomic N6-methyladenosine promotes expression of genes important for chromosome maintenance in bacteria [pacbio_DnmA]

| PRJNA540996 | ENA

Genomic N6-methyladenosine promotes expression of genes important for chromosome maintenance in bacteria [pacbio_DnmA2]

Project description:Genomic N6-methyladenosine promotes expression of genes important for chromosome maintenance in bacteria [pacbio_DnmA2]

| PRJNA540997 | ENA

The RNA N6-Methyladenosine Methyltransferase METTL3 Promotes the Progression of Kidney Cancer via N6-Methyladenosine-Dependent Translational Enhancement of ABCD1.

Project description:The role of N6-methyladenosine (m6A)-modifying proteins in cancer progression depends on the cell type and mRNA affected. However, the biological role and underlying mechanism of m6A in kidney cancer is limited. Here, we discovered the variability in m6A methyltransferase METTL3 expression was significantly increased in clear cell renal cell carcinoma (ccRCC) the most common subtype of renal cell carcinoma (RCC), and high METTL3 expression predicts poor prognosis in ccRCC patients using a dataset from The Cancer Genome Atlas (TCGA). Importantly, knockdown of METTL3 in ccRCC cell line impaired both cell migration capacity and tumor spheroid formation in soft fibrin gel, a mechanical method for selecting stem-cell-like tumorigenic cells. Consistently, overexpression of METTL3 but not methyltransferase activity mutant METTL3 can promote cell migration, spheroid formation in cell line and tumor growth in xenograft model. Transcriptional profiling of m6A in ccRCC tissues identified the aberrant m6A transcripts were enriched in cancer-related pathways. Further m6A-sequencing of METTL3 knockdown cells and functional studies confirmed that translation of ABCD1, an ATP-binding cassette (ABC) transporter of fatty acids, was inhibited by METTL3 in m6A-dependent manner. Moreover, knockdown of ABCD1 in ccRCC cells decreased cancer cell migration and spheroid formation, and upregulation of ABCD1 acts as an adverse prognosis factor of kidney cancer patients. In summary, our study identifies that METTL3 promotes ccRCC progression through m6A modification-mediated translation of ABCD1, providing an epitranscriptional insight into the molecular mechanism in kidney cancer.

| S-EPMC8496489 | biostudies-literature

Arginine methylation of METTL14 promotes RNA N6-methyladenosine modification

Project description:Both mRNA and proteins can be modified through addition of methyl groups. For example, addition of N6-methyladenosine (m6A) to mRNAs is critical for human development and health. Post-translational methylation of proteins can impact the dynamic regulation of enzymatic activity. Here we sought to explore the nexus of transcriptional and post-translational methylation by studying the role of methylation of the core methyltransferase METTL3/METTL14 in m6A regulation. We found by mass spectrometry that METTL14 arginine 255 (R255) is methylated (R255me). Global mRNA m6A levels were greatly decreased in METTL14 R255K mutant mouse embryonic stem cells (mESCs). We further found that R255me greatly enhances the interaction of METTL3/METTL14 with WTAP and promotes the binding of the complex to substrate RNA.

2021-05-14 | GSE164047 | GEO

RNA N6-methyladenosine demethylase FTO promotes breast tumor progression through inhibiting BNIP3.

Project description:BackgroundN6-methyladenosine (m6A) modification is the most pervasive modification in mRNA, and has been considered as a new layer of epigenetic regulation on mRNA processing, stability and translation. Despite its functional significance in various physiological processes, the role of the m6A modification involved in breast cancer is yet fully understood.MethodsWe used the m6A-RNA immunoprecipitation sequencing to identify the potential targets in breast cancer. To determine the underlying mechanism for the axis of FTO-BNIP3, we performed a series of in vitro and in vivo assays in 3 breast cancer cell lines and 36 primary breast tumor tissues and 12 adjunct tissues.ResultsWe showed that FTO, a key m6A demethylase, was up-regulated in human breast cancer. High level of FTO was significantly associated with lower survival rates in patients with breast cancer. FTO promoted breast cancer cell proliferation, colony formation and metastasis in vitro and in vivo. We identified BNIP3, a pro-apoptosis gene, as a downstream target of FTO-mediated m6A modification. Epigenetically, FTO mediated m6A demethylation in the 3'UTR of BNIP3 mRNA and induced its degradation via an YTHDF2 independent mechanism. BNIP3 acts as a tumor suppressor and is negatively correlated with FTO expression in clinical breast cancer patients. BNIP3 dramatically alleviated FTO-dependent tumor growth retardation and metastasis.ConclusionsOur findings demonstrate the functional significance of the m6A modification in breast cancer, and suggest that FTO may serve as a novel potential therapeutic target for breast cancer.

| S-EPMC6437932 | biostudies-literature

RNA N6‑methyladenosine methyltransferase WTAP promotes the differentiation of endothelial progenitor cells.

Project description:N6-methyladenosine (m6A) serves a critical role in regulating gene expression and has been associated with various diseases; however, its role in the differentiation of endothelial progenitor cells (EPCs) remains unclear. The present study used liquid chromatography with tandem mass spectrometry and immunofluorescence assays to quantify the levels of m6A in human peripheral blood-derived EPCs (HPB-EPCs) before and after differentiation into mature cells. The present study performed Cell Counting Kit 8, Transwell, and tube formation assays to determine the effects of overexpression and knockdown of Wilms' tumor 1-associated protein (WTAP) on HPB-EPCs. The results revealed that the level of m6A modification was significantly increased during HPB-EPCs differentiation, and WTAP exhibited the most significant alteration among the enzymes involved in m6A regulation. When WTAP was overexpressed in HPB-EPCs, cell proliferation, invasion, and the formation of tubes were improved, whereas WTAP knockdown yielded the opposite effects. In conclusion, the present study highlighted the involvement of m6A in regulating EPC differentiation, with WTAP acting as a promoter of EPC differentiation.

| S-EPMC10433437 | biostudies-literature

N6-methyladenosine methyltransferase METTL3 promotes colorectal cancer cell proliferation through enhancing MYC expression.

Project description:N6-methyladenosine (m6A) modification is the most common chemical modification in eukaryotic mRNA, which plays a crucial role in regulating mRNA stability, splicing, and translation. METTL3 (methyltransferase like 3), a major RNA N6-adenosine methyltransferase, has been reported to participate in the progression of many cancers. However, its function in colorectal cancer (CRC) remains largely unknown. In this study, we revealed that METTL3 played an oncogenic role in CRC. We found that METTL3 was significantly upregulated in CRC, using quantitative real-time PCR, western blotting, and immunohistochemical staining, and upregulation of METTL3 was associated with clinicopathological features. Functionally, knockdown of METTL3 suppressed CRC cell proliferation in vitro and in vivo. In contrast, overexpression of METTL3 promoted the growth of CRC cells both in vitro and in vivo. Mechanistically, METTL3 exerted its function through enhancing MYC expression, at least partially in an m6A-IGF2BP1-dependent manner. In conclusion, we found that METTL3 was frequently upregulated in human CRC and promoted CRC progression though enhancing MYC expression. This provided new insights into the molecular mechanisms underlying the development of colorectal cancer.

| S-EPMC7270026 | biostudies-literature

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