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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 Bacillus subtilis PY79

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]

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N6-methyladenosine RNA modification promotes viral genomic RNA stability and infection.

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N6-methyladenosine mRNA methylation is important for the light response in soybean.

Project description:N6-methyladenosine (m6A) modification of messenger RNA (mRNA) is the most prevalent and abundant modification in eukaryotic mRNA and posttranscriptionally modulates the transcriptome at almost all stages of mRNA metabolism. In plants, m6A is crucial for embryonic-phase growth, flowering time control, microspore generation and fruit maturation. However, the role of m6A in plant responses to light, the most important environmental stimulus, remains unexplored. Here, we profile the m6A transcriptome of Williams 82, a soybean cultivar, and reveal that m6A is highly conserved and plays an important role in the response to light stimuli in soybean. Similar to the case in Arabidopsis, m6A in soybean is enriched not only around the stop codon and within the 3'UTR but also around the start codon. Moreover, genes with methylation occurring in the 3'UTR have higher expression levels and are more prone to alternative splicing. The core genes in the light signaling pathway, GmSPA1a, GmPRR5e and GmBIC2b, undergo changes in methylation modification and transcription levels in response to light. KEGG pathway analysis revealed that differentially expressed genes with differential m6A peaks were involved in the "photosynthesis" and "circadian rhythm" pathways. Our results highlight the important role played by epitranscriptomic mRNA methylation in the light response in soybean and provide a solid basis for determining the functional role of light on RNA m6A modification in this plant.

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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.

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Project description:Vasculogenic mimicry (VM) has been reported to accelerate angiogenesis in malignant tumors, yet the mechanism underlying VM has not been fully elucidated. N6-methyladenosine (m6A) mainly modulates mRNA fate and affects multiple tumorigenesis. Here, we aimed to investigate m6A-modified HOXA transcript antisense RNA myeloid-specific 1 (HOTAIRM1) in the regulation of glioma-associated VM formation. Gene expression was analyzed by quantitative RT-PCR. Cell viability, metastases, and VM formation capacity were determined by CCK-8, migration and invasion, as well as tube formation assays, respectively. The function and mechanisms of m6A-modified HOTAIRM1 were defined through liquid chromatography-tandem mass spectrometry m6A quantification, methylated RNA immunoprecipitation sequencing, RNA stability assays, and RNA pull-down experiments. A glioma xenograft mouse model was further established for VM evaluation in vivo. The results showed that HOTAIRM1, methyltransferase-like 3 (METTL3), and insulin-like growth factor binding protein 2 (IGFBP2) were upregulated in glioma tissues and cell lines. HOTAIRM1 functions as an oncogene in glioma progression; however, knockdown of HOTAIRM1 significantly reduced cell viability, migration, invasion, and VM formation. Notably, METTL3-dependent m6A modification enhanced HOTAIRM1 mRNA stability, whereas knockdown of METTL3 deficiency significantly suppressed VM in glioma. Moreover, HOTAIRM1 was found to bind IGFBP2, and HOTAIRM1 deficiency blocked glioma progression and VM formation in vivo. Our results indicated that METTL3-dependent m6A-modified HOTAIRM1 promoted VM formation in glioma.

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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.

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