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Transcriptome-wide N6-methyladenine methylation in granulosa cells of women with decreased ovarian reserve

ABSTRACT: Transcriptome-wide N6-methyladenine methylation in granulosa cells of women with decreased ovarian reserve

PROVIDER: PRJNA750720 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15295306_1.fastq.gz	Fastqsanger.gz
	SRR15295306_2.fastq.gz	Fastqsanger.gz
	SRR15295307_1.fastq.gz	Fastqsanger.gz
	SRR15295307_2.fastq.gz	Fastqsanger.gz
	SRR15295308_1.fastq.gz	Fastqsanger.gz

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Transcriptome-wide N6-methyladenine methylation in granulosa cells of women with decreased ovarian reserve.

Project description:BackgroundThe emerging epitranscriptome plays an essential role in female fertility. As the most prevalent internal mRNA modification, N6-methyladenine (m6A) methylation regulate mRNA fate and translational efficiency. However, whether m6A methylation was involved in the aging-related ovarian reserve decline has not been investigated. Herein, we performed m6A transcriptome-wide profiling in the ovarian granulosa cells of younger women (younger group) and older women (older group).Resultsm6A methylation distribution was highly conserved and enriched in the CDS and 3'UTR region. Besides, an increased number of m6A methylated genes were identified in the older group. Bioinformatics analysis indicated that m6A methylated genes were enriched in the FoxO signaling pathway, adherens junction, and regulation of actin cytoskeleton. A total of 435 genes were differently expressed in the older group, moreover, 58 of them were modified by m6A. Several specific genes, including BUB1B, PHC2, TOP2A, DDR2, KLF13, and RYR2 which were differently expressed and modified by m6A, were validated using qRT-PCR and might be involved in the decreased ovarian functions in the aging ovary.ConclusionsHence, our finding revealed the transcriptional significance of m6A modifications and provide potential therapeutic targets to promote fertility reservation for aging women.

| S-EPMC8961905 | biostudies-literature

Transcriptome-wide N6-methyladenine methylation in granulosa cells of women with decreased ovarian reserve

Project description:The results revealed the transcriptional significance of m6A modifications and provide potential therapeutic targets to promote fertility reservation for aging women.

2022-04-01 | GSE181106 | GEO

N6-Methyladenine DNA Modification in Human Genome

Project description:In human cells, 5-methylcytosine (5mC) DNA modification plays an important role in gene regulation. However, N6-methyladenine (6mA) DNA modification, which is predominantly present in prokaryotes, is considered to be absent in human genomic DNA. Here, using single molecule real-time (SMRT) sequencing on human blood, we show that DNA 6mA modification is extensively present in human genome, accounting for ~0.051% of the total adenines. [G/C]AGG[C/T] was the most significant motif associated with 6mA modification. 6mA sites are enriched in the exon coding regions and are associated with transcriptional activation. DNA N6-methyladenine and N6-demethyladenine modification in human are mediated by methyltransferase N6AMT1 and demethylase ALKBH1, respectively. The 6mA abundance is significantly lower in cancer tissues compared to adjacent normal tissues, which is accompanied with decreased N6AMT1 and increased ALKBH1 levels. Decrease of 6mA modification level stimulated tumorigenesis in human. Collectively, our results demonstrate that 6mA DNA modification is present in human tissues, and we describe a potential role of the N6AMT1/ALKBH1-6mA regulatory axis in the progression of human cancer.

2017-10-02 | GSE104475 | GEO

N6-methyladenine DNA Modification in Glioblastoma

Project description:N6-methyladenine DNA Modification in Glioblastoma

| PRJNA484394 | ENA

N6-Methyladenine DNA Modification in Human Genome

Project description:N6-Methyladenine DNA Modification in Human Genome

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N6-methyladenine DNA Modification in Glioblastoma [ATAC-seq]

Project description:Genetic drivers of cancer can be dysregulated through epigenetic modifications of DNA. While the critical role of DNA 5-methylcytosine (5mC) in the regulation of transcription is recognized, the functions of other non-canonical DNA modifications remain obscure. Here, we report the identification of novel N(6)-methyladenine (N6-mA) DNA modifications in human tissues and implicate this epigenetic regulation in human disease, the highly malignant brain cancer, glioblastoma. Glioblastoma upregulates N6-mA levels, which co-localize with heterochromatic histone modifications, namely H3K9me3. N6-mA levels are dynamically regulated by the DNA demethylase, ALKBH1, to transcriptionally silence oncogenic pathways through decreasing chromatin accessibility. Targeting the N6-mA regulator, ALKBH1, in patient-derived human glioblastoma models inhibited tumor cell proliferation and extended survival of tumor-bearing mice, supporting this novel DNA modification as a potential new molecular therapeutic target for glioblastoma. Collectively, our results uncover a novel epigenetic node in cancer through the DNA modification, N6-mA.

2018-11-01 | GSE118092 | GEO

N6-methyladenine DNA Modification in Glioblastoma [RNA-seq]

Project description:Genetic drivers of cancer can be dysregulated through epigenetic modifications of DNA. While the critical role of DNA 5-methylcytosine (5mC) in the regulation of transcription is recognized, the functions of other non-canonical DNA modifications remain obsure. Here, we report the identification of novel N(6)-methyladenine (N6-mA) DNA modifications in human tissues and implicate this epigenetic regulation in human disease, the highly malignant brain cancer, glioblastoma. Glioblastoma upregulates N6-mA levels, which co-localize with heterochromatic histone modifications, namely H3K9me3. N6-mA levels are dynamically regulated by the DNA demethylase, ALKBH1, to transcriptionally silence oncogenic pathways through decreasing chromatin accessibility. Targeting the N6-mA regulator, ALKBH1, in patient-derived human glioblastoma models inhibited tumor cell proliferation and extended survival of tumor-bearing mice, supporting this novel DNA modification as a potential new molecular therapeutic target for glioblastoma. Collectively, our results uncover a novel epigenetic node in cancer through the DNA modification, N6-mA.

2018-11-01 | GSE117632 | GEO

Identify the interplay between N6-methyladenine and gene regulation under hypoxia by randomized empirical model (RNA-seq)

Project description:In this study, we employed RNA-seq to investigate the role of N6-methyladenine (6mA) in chromatin accessibility under hypoxic conditions.

2024-11-21 | GSE260872 | GEO

Characterization of eukaryotic DNA N6-methyladenine by a highly sensitive restriction enzyme-assisted sequencing

Project description:To interrogate single-base resolution 6mA sites in the genome-wide, we develop DA-6mA-seq (DpnI-Assisted N6-methylAdenine sequencing), an optimized sequencing method taking advantage of restriction enzyme DpnI, which exclusively cleaves methylated adenine sites. We find DpnI also recognizes other sequence motifs besides the canonical GATC restriction sites, largely expanding the application range of this method. DA-6mA-seq requires less starting material and lower sequencing depth than previous methods, but achieves higher sensitivity, providing a good strategy to identify 6mA in large genome with a low abundance of 6mA. We rebuild the 6mA maps of Chlamydomonas by DA-6mA-seq and then apply this method to another two eukaryotic organisms, Plasmodium and Penicillium. Further analysis reveals most 6mA sites are symmetric at various sequence contexts, suggesting 6mA may function as a new heritable epigenetic mark in eukaryotes. A new sequencing method is developed to detect 6mA in eukaryotes

2016-04-12 | E-GEOD-74430 | biostudies-arrayexpress

N6-methyladenine DNA Modification in Glioblastoma [RNA-seq]

Project description:N6-methyladenine DNA Modification in Glioblastoma [RNA-seq]

| PRJNA482757 | ENA