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Genome wide 6mA modification change upon mitochondial stress in C.elegans

ABSTRACT: We discovered 364 peaks enrichment change in wild-type C.elegans genome by 6mA MeDIP-seq, which indicated those genes response to mitochondrial stress and may function in mitochondrial stress response.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE118268 | GEO | 2018/09/27

REPOSITORIES: GEO

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Genome wide 6mA modification change upon mitochondial stress in C.elegans

Project description:Genome wide 6mA modification change upon mitochondial stress in C.elegans

| PRJNA484980 | ENA

Genome wide DNA 6mA methylome and transcriptome change upon mitochondrial stress in C.elegans

Project description:Genome wide DNA 6mA methylome and transcriptome change upon mitochondrial stress in C.elegans

| PRJNA484977 | ENA

Transcriptome wide change upon mitochondial stress in C.elegans

Project description:We discovered 5446 genes expression change (4218 genes from P0 to F2) in wild-type C.elegans transcriptome compared to DAMT-1 mutant upon mitochondrial stress by RNA-seq, which indicated those genes response to mitochondrial stress and may function in mitochondrial stress response.

2018-09-27 | GSE118175 | GEO

Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [MeDIP-seq]

Project description:Background: DNA N6-methyladenosine (6mA) as a novel epigenetic signaling modification in humans and has been implicated in progression and tumorigenesis of several cancers. However, the function and mechanisms of 6mA in breast cancer (BC), the most common cancer among women, are unclear. Methods: The clinical role of 6mA was investigated by immunohistochemical (IHC) staining and Kaplan-Meier analysis of BC and their normal tissues. 6mA immunoprecipitation (IP) sequencing, mRNA sequencing and bioinformatics analysis were used to screen and validate the direct targets of 6mA. Results: Decreases in N6AMT1 correlated with the extent of 6mA in BC tissues and predicted a worse overall survival of BC patients. Knockdown N6AMT1 markedly reduced 6mA in DNA and promoted the proliferation and migration of BC in vivo and in vitro, whereas overexpression of N6AMT1 had the opposite effect, indicating N6AMT1 is a functional methyltransferase for DNA 6mA and relates with gene transcription. Critical negative regulators of the cell cycle, such as RB1, P21, REST and TP53 were identified as targets of N6AMT1 in BC. Conclusion: These results suggest N6AMT1 enhances DNA 6mA levels to repress tumor progression via transcriptional regulation of cell cycle inhibitors.

2022-03-31 | GSE166580 | GEO

Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [RNA-seq]

2022-03-31 | GSE166576 | GEO

Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [MeDIP-seq]

Project description:Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [MeDIP-seq]

| PRJNA701301 | ENA

Transcriptome wide change upon mitochondial stress in C.elegans

Project description:Transcriptome wide change upon mitochondial stress in C.elegans

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Effect of misregulation of mitochondrial 6mA on gene expression in C. elegans

Project description:In virtually all eukaryotes, the mitochondrial genome (mitochondrial DNA, mtDNA) encodes proteins necessary for oxidative phosphorylation (OXPHOS) and the RNA machinery required for their synthesis inside the mitochondria. Appropriate regulation of mtDNA copy number and expression is essential for ensuring the correct stoichiometric formation of OXPHOS complexes assembled from both nuclear- and mtDNA-encoded subunits. The mechanisms of mtDNA regulation are not completely understood but are essential to organismal viability and lifespan. Here, using multiple approaches, we identify the presence of N6-methylation of adenosine (6mA) on the mtDNA of diverse animal and plant species. Importantly, we also demonstrate that this modification is regulated in C. elegans by the DNA methyltransferase DAMT-1, and DNA demethylase ALKB-1, which localize to mitochondria. Misregulation of mtDNA 6mA through targeted overexpression of these enzymatic activities inappropriately alters mtDNA copy number and transcript levels, impairing OXPHOS function and producing increased oxidative stress, as well as a shortened lifespan. Compounding defects in mtDNA regulation, reductions in mtDNA 6mA methylation promote the propagation of a deleterious mitochondrial genome across generations. Together, these results reveal that mtDNA 6mA is highly conserved among eukaryotes and regulates lifespan by influencing mtDNA copy number, expression, and heritable mutation levels in vivo.

2024-08-11 | GSE272419 | GEO

Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression

Project description:Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression

| PRJNA701297 | ENA

Abundant DNA 6mA methylation during early embryogenesis of zebrafish

Project description:DNA N6-methyldeoxyadenosine (6mA) is a well known prokaryotic DNA modification and has been shown to exist and play epigenetic roles in eukaryotic DNA. Here we report that 6mA accumulates up to 0.1% of total deoxyadenosine during early embryogenesis of vertebates, but diminishes with progression of the embryo development. During this process most 6mA locates in repetitive regions of the genome.

2016-10-10 | GSE76740 | GEO

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