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Identify the interplay between N6-methyladenine and gene regulation under hypoxia by randomized empirical model (6mA)

ABSTRACT: Identify the interplay between N6-methyladenine and gene regulation under hypoxia by randomized empirical model (6mA)

PROVIDER: PRJNA1083882 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28237068.fastq.gz	Fastqsanger.gz
	SRR28229672.fastq.gz	Fastqsanger.gz
	SRR28229676.fastq.gz	Fastqsanger.gz

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Identify the interplay between N6-methyladenine and gene regulation under hypoxia by randomized empirical model (6mA)

Project description:This dataset encompasses comprehensive analyses of the epigenetic mark N6-methyladenine (6mA) in human cell lines, focusing on its role under hypoxic conditions and its association with cancer progression. Addressing the challenge of 6mA's low abundance in mammals, we have innovated the 6mA-ChIP-exo-5.1 method. This technique enhances the sensitivity and accuracy of 6mA detection, employing exonuclease-dependent antibody-based approaches combined with whole genome amplification (WGA) to minimize potential noise and false positives.

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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.

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

Project description:In this study, we employed ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) to investigate the role of N6-methyladenine (6mA) in chromatin accessibility under hypoxic conditions.

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

Project description:In this study, we employed ChIP-seq for histone modifications related to gene activation, such as H3K4me1, H3K4me3, and H3K27Ac, to investigate the role of N6-methyladenine (6mA) in chromatin accessibility under hypoxic conditions.

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

Project description:Identify the interplay between N6-methyladenine and gene regulation under hypoxia by randomized empirical model (ATAC-seq)

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

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

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

Project description:Identify the interplay between N6-methyladenine and gene regulation under hypoxia by randomized empirical model (ChIP-seq)

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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

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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.

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